start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=1
article-no=
start-page=234
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rotenone targets midbrain astrocytes to produce glial dysfunction-mediated dopaminergic neurodegeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Exposure to pesticides, such as rotenone or paraquat, is an environmental factor that plays an important role in the pathogenesis of Parkinson's disease (PD). Rotenone induces PD-like pathology and is therefore used to develop parkinsonian animal models. Dopaminergic neurotoxicity caused by rotenone has been attributed to the inhibition of mitochondrial complex I, oxidative stress and neuroinflammation; however, the mechanisms underlying selective dopaminergic neurodegeneration by rotenone remain unclear. To resolve this, we focused on glial diversity and examined whether the brain region-specific glial response to rotenone could determine the vulnerability of dopaminergic neurons using primary cultured neurons, astrocytes and microglia from the midbrain and striatum of rat embryos and rotenone-injected PD model mice. Direct neuronal treatment with low-dose rotenone failed to damage dopaminergic neurons. Conversely, rotenone exposure in the presence of midbrain astrocyte and microglia or conditioned media from rotenone-treated midbrain glial cultures containing astrocytes and microglia produced dopaminergic neurotoxicity, but striatal glia did not. Surprisingly, conditioned media from rotenone-treated midbrain astrocytes or microglia monocultures did not affect neuronal survival. We also demonstrated that rotenone targeted midbrain astrocytes prior to microglia to induce dopaminergic neurotoxicity. Rotenone-treated astrocytes produced secreted protein acidic and rich in cysteine (SPARC) extracellularly, which induced microglial proliferation, increase in IL-1β and TNF-α, and NF-κB (p65) nuclear translocation in microglia, resulting in dopaminergic neurodegeneration. In addition, rotenone exposure caused the secretion of NFAT-related inflammatory cytokines and a reduction in the level of an antioxidant metallothionein (MT)-1 from midbrain glia. Furthermore, we observed microglial proliferation and a decrease in the number of MT-positive astrocytes in the substantia nigra, but not the striatum, of low-dose rotenone-injected PD model mice. Our data highlight that rotenone targets midbrain astrocytes, leading to SPARC secretion, which promotes the neurotoxic conversion of microglia and leads to glial dysfunction-mediated dopaminergic neurodegeneration.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IsookaNami
en-aut-sei=Isooka
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KikuokaRyo
en-aut-sei=Kikuoka
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImafukuFuminori
en-aut-sei=Imafuku
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TomimotoKana
en-aut-sei=Tomimoto
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SogawaChiharu
en-aut-sei=Sogawa
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SogawaNorio
en-aut-sei=Sogawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Food and Health Sciences, Faculty of Environmental Studies, Hiroshima Institute of Technology
kn-affil=

affil-num=9
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Pharmacotherapy, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=11
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Rotenone
kn-keyword=Rotenone
en-keyword=Astrocyte
kn-keyword=Astrocyte
en-keyword=Microglia
kn-keyword=Microglia
en-keyword=SPARC
kn-keyword=SPARC
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=1
article-no=
start-page=4
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Differentially Expressed Nedd4-binding Protein Ndfip1 Protects Neurons Against Methamphetamine-induced Neurotoxicity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To identify factors involved in methamphetamine (METH) neurotoxicity, we comprehensively searched for genes which were differentially expressed in mouse striatum after METH administration using differential display (DD) reverse transcription-PCR method and sequent single-strand conformation polymorphism analysis, and found two DD cDNA fragments later identified as mRNA of Nedd4 (neural precursor cell expressed developmentally downregulated 4) WW domain-binding protein 5 (N4WBP5), later named Nedd4 family-interacting protein 1 (Ndfip1). It is an adaptor protein for the binding between Nedd4 of ubiquitin ligase (E3) and target substrate protein for ubiquitination. Northern blot analysis confirmed drastic increases in Ndfip1 mRNA in the striatum after METH injections, and in situ hybridization histochemistry showed that the mRNA expression was increased in the hippocampus and cerebellum at 2 h-2 days, in the cerebral cortex and striatum at 18 h-2 days after single METH administration. The knockdown of Ndfip1 expression with Ndfip1 siRNA significantly aggravated METH-induced neurotoxicity in the cultured monoaminergic neuronal cells. These results suggest that drastic increases in Ndfip1 mRNA is compensatory reaction to protect neurons against METH-induced neurotoxicity.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=CadetJean Lud
en-aut-sei=Cadet
en-aut-mei=Jean Lud
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Molecular Neuropsychiatry Section, Intramural Research Program, NIH/ NIDA
kn-affil=
en-keyword=Methamphetamine
kn-keyword=Methamphetamine
en-keyword=Neurotoxicity
kn-keyword=Neurotoxicity
en-keyword=Nedd4
kn-keyword=Nedd4
en-keyword=Ndfip1
kn-keyword=Ndfip1
en-keyword=Differential display
kn-keyword=Differential display
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=2
article-no=
start-page=102575
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical and microbiological characteristics of high-level daptomycin-resistant Corynebacterium species: A systematic scoping review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Corynebacterium species potentially develop high-level daptomycin resistance (HLDR) shortly after daptomycin (DAP) administration. We aimed to investigate the clinical and microbiological characteristics of HLDR Corynebacterium infections.<br>
Methods: We first presented a clinical case accompanied by the results of a comprehensive genetic analysis of the isolate, and then performed a systematic scoping review. Based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews, we searched for articles with related keywords, including “Corynebacterium”, “Daptomycin", and "Resistance”, in the MEDLINE and Web of Science databases from the database inception to October 25, 2024. Clinical case reports and research articles documenting the isolation of HLDR Corynebacterium species, defined by a minimum inhibitory concentration of DAP at ≥256 μg/mL, were deemed eligible for this review.<br>
Results: Of 80 articles screened, seven case reports detailing eight cases of HLDR Corynebacterium infections, as well as five research articles, were included. C. striatum was the most common species (7/9 cases, 77.8 %), and prosthetic device-associated infections accounted for 66.7 % of the cases. Duration of DAP administration before the emergence of HLDR isolates ranged from 5 days to 3 months; three-quarters of the cases developed within 17 days. Three HLDR isolates were genetically confirmed to have an alteration in pgsA2. The majority of the patients were treated with either glycopeptides or linezolid, with favorable outcomes. In vitro experiments confirmed that C. striatum strains acquire the HLDR phenotype at higher rates (71 %–100 %) within 24 h of incubation, compared to other Corynebacterium strains.<br>
Conclusion: DAP monotherapy, especially for prosthetic device-associated infections, can result in the development of HLDR Corynebacterium. Additional research is warranted to investigate the clinical implications of this potentially proliferating antimicrobial resistant pathogen.
en-copyright=
kn-copyright=

en-aut-name=FukushimaShinnosuke
en-aut-sei=Fukushima
en-aut-mei=Shinnosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GotohKazuyoshi
en-aut-sei=Gotoh
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsujiShuma
en-aut-sei=Tsuji
en-aut-mei=Shuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IioKoji
en-aut-sei=Iio
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AkazawaHidemasa
en-aut-sei=Akazawa
en-aut-mei=Hidemasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsushitaOsamu
en-aut-sei=Matsushita
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Infectious Diseases, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Medical Laboratory Science, Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Laboratory Science, Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=5
en-affil=Microbiology Division, Clinical Laboratory, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Infectious Diseases, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Infectious Diseases, Okayama University Hospital
kn-affil=
en-keyword=Antimicrobial resistance
kn-keyword=Antimicrobial resistance
en-keyword=Corynebacterium
kn-keyword=Corynebacterium
en-keyword=Daptomycin
kn-keyword=Daptomycin
en-keyword=High-level daptomycin resistance
kn-keyword=High-level daptomycin resistance
en-keyword=pgsA2
kn-keyword=pgsA2
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=121
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pure argyrophilic grain disease revisited: independent effects on limbic, neocortical, and striato-pallido-nigral degeneration and the development of dementia in a series with a low to moderate Braak stage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Agyrophilic grains (AGs) are age-related limbic-predominant lesions in which four-repeat tau is selectively accumulated. Because previous methodologically heterogeneous studies have demonstrated inconsistent findings on the relationship between AGs and dementia, whether AGs affect cognitive function remains unclear. To address this question, we first comprehensively evaluated the distribution and quantity of Gallyas-positive AGs and the severity of neuronal loss in the limbic, neocortical, and subcortical regions in 30 cases of pure argyrophilic grain disease (pAGD) in Braak stages I-IV and without other degenerative diseases, and 34 control cases that had only neurofibrillary tangles with Braak stages I-IV and no or minimal A beta deposits. Then, we examined whether AGs have independent effects on neuronal loss and dementia by employing multivariate ordered logistic regression and binomial logistic regression. Of 30 pAGD cases, three were classified in diffuse form pAGD, which had evident neuronal loss not only in the limbic region but also in the neocortex and subcortical nuclei. In all 30 pAGD cases, neuronal loss developed first in the amygdala, followed by temporo-frontal cortex, hippocampal CA1, substantia nigra, and finally, the striatum and globus pallidus with the progression of Saito AG stage. In multivariate analyses of 30 pAGD and 34 control cases, the Saito AG stage affected neuronal loss in the amygdala, hippocampal CA1, temporo-frontal cortex, striatum, globus pallidus, and substantia nigra independent of the age, Braak stage, and limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) stage. In multivariate analyses of 23 pAGD and 28 control cases that lacked two or more lacunae and/or one or more large infarctions, 100 or more AGs per x 400 visual field in the amygdala (OR 10.02, 95% CI 1.12-89.43) and hippocampal CA1 (OR 12.22, 95% CI 1.70-87.81), and the presence of AGs in the inferior temporal cortex (OR 8.18, 95% CI 1.03-65.13) affected dementia independent of age, moderate Braak stages (III-IV), and LATE-NC. Given these findings, the high density of limbic AGs and the increase of AGs in the inferior temporal gyrus may contribute to the occurrence of dementia through neuronal loss, at least in cases in a low to moderate Braak stage.
en-copyright=
kn-copyright=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiTomoko
en-aut-sei=Miki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaChikako
en-aut-sei=Ikeda
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyashitaAkinori
en-aut-sei=Miyashita
en-aut-mei=Akinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkeuchiTakeshi
en-aut-sei=Ikeuchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishikawaNaoto
en-aut-sei=Nishikawa
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakenoshitaShintaro
en-aut-sei=Takenoshita
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SudoKoichiro
en-aut-sei=Sudo
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Okayama University Medical School 
kn-affil=

affil-num=4
en-affil=Okayama University Medical School 
kn-affil=

affil-num=5
en-affil=Department of Neurology, National Hospital Organization Minami Okayama Medical Center
kn-affil=

affil-num=6
en-affil=Okayama University Medical School 
kn-affil=

affil-num=7
en-affil=Dementia Research Project, Tokyo Metropolitan Institute of Medical Science
kn-affil=

affil-num=8
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=9
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=10
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Psychiatry, Tosa Hospital
kn-affil=

affil-num=13
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Argyrophilic grain
kn-keyword=Argyrophilic grain
en-keyword=Globus pallidus
kn-keyword=Globus pallidus
en-keyword=Hippocampal sclerosis
kn-keyword=Hippocampal sclerosis
en-keyword=Striatum
kn-keyword=Striatum
en-keyword=Substantia nigra
kn-keyword=Substantia nigra
en-keyword=Subthalamic nucleus
kn-keyword=Subthalamic nucleus
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=2
article-no=
start-page=594
end-page=603
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202303
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Continuous vagus nerve stimulation exerts beneficial effects on rats with experimentally induced Parkinson's disease: Evidence suggesting involvement of a vagal afferent pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Vagus nerve stimulation (VNS) exerts neuroprotective and anti-inflammatory effects in preclinical models of central nervous system disorders, including Parkinson's disease (PD). VNS setting applied for experimental models is limited into single-time or intermittent short-duration stimulation. We developed a VNS device which could deliver continuous stimulation for rats. To date, the effects of vagal afferent-or efferent-selective stimulation on PD using continuous electrical stimulation remains to be determined. <br>
Objective: To investigate the effects of continuous and selective stimulation of vagal afferent or efferent fiber on Parkinsonian rats. <br>
Methods: Rats were divided into 5 group: intact VNS, afferent VNS (left VNS in the presence of left caudal vagotomy), efferent VNS (left VNS in the presence of left rostral vagotomy), sham, vagotomy. Rats un-derwent the implantation of cuff-electrode on left vagus nerve and 6-hydroxydopamine administration into the left striatum simultaneously. Electrical stimulation was delivered just after 6-OHDA adminis-tration and continued for 14 days. In afferent VNS and efferent VNS group, the vagus nerve was dissected at distal or proximal portion of cuff-electrode to imitate the selective stimulation of afferent or efferent vagal fiber respectively. <br>
Results: Intact VNS and afferent VNS reduced the behavioral impairments in cylinder test and methamphetamine-induced rotation test, which were accompanied by reduced inflammatory glial cells in substantia nigra with the increased density of the rate limiting enzyme in locus coeruleus. In contrast, efferent VNS did not exert any therapeutic effects. <br>
Conclusion: Continuous VNS promoted neuroprotective and anti-inflammatory effect in experimental PD, highlighting the crucial role of the afferent vagal pathway in mediating these therapeutic outcomes.
en-copyright=
kn-copyright=

en-aut-name=HosomotoKakeru
en-aut-sei=Hosomoto
en-aut-mei=Kakeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KamedaMasahiro
en-aut-sei=Kameda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SasadaSusumu
en-aut-sei=Sasada
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KinIttetsu
en-aut-sei=Kin
en-aut-mei=Ittetsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KuwaharaKen
en-aut-sei=Kuwahara
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawauchiSatoshi
en-aut-sei=Kawauchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KawaiKoji
en-aut-sei=Kawai
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TanimotoShun
en-aut-sei=Tanimoto
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=BorlonganCesario V.
en-aut-sei=Borlongan
en-aut-mei=Cesario V.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine
kn-affil=

affil-num=16
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
en-keyword=Vagus nerve stimulation
kn-keyword=Vagus nerve stimulation
en-keyword=Afferent pathway
kn-keyword=Afferent pathway
en-keyword=Locus coeruleus
kn-keyword=Locus coeruleus
en-keyword=Dopamine
kn-keyword=Dopamine
en-keyword=Noradrenaline
kn-keyword=Noradrenaline
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=10
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synergistic therapeutic effects of intracerebral transplantation of human modified bone marrow-derived stromal cells (SB623) and voluntary exercise with running wheel in a rat model of ischemic stroke
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background　Mesenchymal stromal cell (MSC) transplantation therapy is a promising therapy for stroke patients. In parallel, rehabilitation with physical exercise could ameliorate stroke-induced neurological impairment. In this study, we aimed to clarify whether combination therapy of intracerebral transplantation of human modified bone marrow-derived MSCs, SB623 cells, and voluntary exercise with running wheel (RW) could exert synergistic therapeutic effects on a rat model of ischemic stroke.<br>
Methods　Wistar rats received right transient middle cerebral artery occlusion (MCAO). Voluntary exercise (Ex) groups were trained in a cage with RW from day 7 before MCAO. SB623 cells (4.0 x 10(5) cells/5 mu l) were stereotactically injected into the right striatum at day 1 after MCAO. Behavioral tests were performed at day 1, 7, and 14 after MCAO using the modified Neurological Severity Score (mNSS) and cylinder test. Rats were euthanized at day 15 after MCAO for mRNA level evaluation of ischemic infarct area, endogenous neurogenesis, angiogenesis, and expression of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF). The rats were randomly assigned to one of the four groups: vehicle, Ex, SB623, and SB623 + Ex groups.<br>
Results　SB623 + Ex group achieved significant neurological recovery in mNSS compared to the vehicle group (p < 0.05). The cerebral infarct area of SB623 + Ex group was significantly decreased compared to those in all other groups (p < 0.05). The number of BrdU/Doublecortin (Dcx) double-positive cells in the subventricular zone (SVZ) and the dentate gyrus (DG), the laminin-positive area in the ischemic boundary zone (IBZ), and the mRNA level of BDNF and VEGF in SB623 + Ex group were significantly increased compared to those in all other groups (p < 0.05).<br>
Conclusions　This study suggests that combination therapy of intracerebral transplantation SB623 cells and voluntary exercise with RW achieves robust neurological recovery and synergistically promotes endogenous neurogenesis and angiogenesis after cerebral ischemia, possibly through a mechanism involving the up-regulation of BDNF and VEGF.
en-copyright=
kn-copyright=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawauchiSatoshi
en-aut-sei=Kawauchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HosomotoKakeru
en-aut-sei=Hosomoto
en-aut-mei=Kakeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SasadaSusumu
en-aut-sei=Sasada
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TajiriNaoki
en-aut-sei=Tajiri
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=BorlonganCesar V.
en-aut-sei=Borlongan
en-aut-mei=Cesar V.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences and Medical School
kn-affil=

affil-num=11
en-affil=Department of Neurosurgery and Brain Repair, Morsani College of Medicine, University of South Florida
kn-affil=

affil-num=12
en-affil=Department of Neurological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Cerebral ischemic infarct
kn-keyword=Cerebral ischemic infarct
en-keyword=Rehabilitation
kn-keyword=Rehabilitation
en-keyword=Regenerative medicine
kn-keyword=Regenerative medicine
en-keyword=SB623
kn-keyword=SB623
en-keyword=Voluntary exercise
kn-keyword=Voluntary exercise
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=23
article-no=
start-page=15412
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Alterations in UPR Signaling by Methylmercury Trigger Neuronal Cell Death in the Mouse Brain
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Methylmercury (MeHg), an environmental toxicant, induces neuronal cell death and injures specific areas of the brain. MeHg is known to induce oxidative and endoplasmic reticulum (ER) stress. The unfolded protein response (UPR) pathway has a dual nature in that it regulates and protects cells from an overload of improperly folded proteins in the ER, whereas excessively stressed cells are eliminated by apoptosis. Oxidative stress/ER stress induced by methylmercury exposure may tilt the UPR toward apoptosis, but there is little in vivo evidence of a direct link to actual neuronal cell death. Here, by using the ER stress-activated indicator (ERAI) system, we investigated the time course signaling alterations of UPR in vivo in the most affected areas, the somatosensory cortex and striatum. In the ERAI-Venus transgenic mice exposed to MeHg (30 or 50 ppm in drinking water), the ERAI signal, which indicates the activation of the cytoprotective pathway of the UPR, was only transiently enhanced, whereas the apoptotic pathway of the UPR was persistently enhanced. Furthermore, detailed analysis following the time course showed that MeHg-induced apoptosis is strongly associated with alterations in UPR signaling. Our results suggest that UPR modulation could be a therapeutic target for treating neuropathy.
en-copyright=
kn-copyright=

en-aut-name=NomuraRyosuke
en-aut-sei=Nomura
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HiraokaHideki
en-aut-sei=Hiraoka
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwawakiTakao
en-aut-sei=Iwawaki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KumagaiYoshito
en-aut-sei=Kumagai
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujimuraMasatake
en-aut-sei=Fujimura
en-aut-mei=Masatake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Cell Medicine, Department of Life Science, Medical Research Institute, Kanazawa Medical University
kn-affil=

affil-num=6
en-affil=Environmental Biology Laboratory, Faculty of Medicine, University of Tsukuba
kn-affil=

affil-num=7
en-affil=Department of Basic Medical Science, National Institute for Minamata Disease
kn-affil=

affil-num=8
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=methylmercury
kn-keyword=methylmercury
en-keyword=neuronal cell death
kn-keyword=neuronal cell death
en-keyword=endoplasmic reticulum stress
kn-keyword=endoplasmic reticulum stress
en-keyword=unfolded protein response
kn-keyword=unfolded protein response
en-keyword=ERAI system
kn-keyword=ERAI system
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=5
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202202
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mouse Model for Optogenetic Genome Engineering
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Optogenetics, a technology to manipulate biological phenomena thorough light, has attracted much attention in neuroscience. Recently, the Magnet System, a photo-inducible protein dimerization system which can control the intracellular behavior of various biomolecules with high accuracy using light was developed. Furthermore, photoactivation systems for controlling biological phenomena are being developed by combining this technique with genome-editing technology (CRISPR/Cas9 System) or DNA recombination technology (Cre-loxP system). Herein, we review the history of optogenetics and the latest Magnet System technology and introduce our recently developed photoactivatable Cre knock-in mice with temporal-, spatial-, and cell-specific accuracy.
en-copyright=
kn-copyright=

en-aut-name=TakaoTomoka
en-aut-sei=Takao
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamadaDaisuke
en-aut-sei=Yamada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakaradaTakeshi
en-aut-sei=Takarada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=optogenetics
kn-keyword=optogenetics
en-keyword=Cre recombinase
kn-keyword=Cre recombinase
END

start-ver=1.4
cd-journal=joma
no-vol=41
cd-vols=
no-issue=2
article-no=
start-page=331
end-page=333
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Detection of in-frame mutation by IS30-family insertion sequence in the phospholipid phosphatidylglycerol synthase gene (pgsA2) of high-level daptomycin-resistant Corynebacterium striatum
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The emergence of high-level daptomycin (DAP)-resistant (HLDR) Corynebacterium striatum has been reported as a result of loss-of-function point mutations or premature stop codon mutations in a responsible gene, pgsA2. We herein describe the novel detection of an HLDR C. striatum clinical isolate, in which IS30-insertion was corroborated to cause destruction of pgsA2 gene. We isolated an HLDR C. striatum from a critically ill patient with underlying mycosis fungoides who had been treated with DAP for ten days. With a sequence investigation, IS30-insertion was discovered to split pgsA2 in the HLDR C. striatum strain, which may cause disrupted phospholipid phosphatidylglycerols (PG) production. Future studies should survey the prevalence of IS-mediated gene inactivation among HLDR C. striatum clinical isolates. 
en-copyright=
kn-copyright=

en-aut-name=GotohKazuyoshi
en-aut-sei=Gotoh
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MayuraI. Putu Bayu
en-aut-sei=Mayura
en-aut-mei=I. Putu Bayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EnomotoYusaku
en-aut-sei=Enomoto
en-aut-mei=Yusaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IioKoji
en-aut-sei=Iio
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsushitaOsamu
en-aut-sei=Matsushita
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Microbiology Division, Clinical Laboratory, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Antimicrobial Resistance
kn-keyword=Antimicrobial Resistance
en-keyword=Daptomycin resistance
kn-keyword=Daptomycin resistance
en-keyword=Corynebacterium striatum
kn-keyword=Corynebacterium striatum
en-keyword=Insertion sequence
kn-keyword=Insertion sequence
en-keyword=pgsA2 gene
kn-keyword=pgsA2 gene
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=19
article-no=
start-page=3155
end-page=3160
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nodal Peripheral T-cell Lymphoma with T Follicular Helper Phenotype Presenting as Chorea During Treatment: A Case Report and Literature Review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 72-year-old man presented with chorea while undergoing treatment for recurrence of nodal peripheral T-cell lymphoma with T follicular helper (TFH) phenotype. An examination by brain N-isopropyl-p-iodoamphetamine (I-123-IMP)-single photon emission computed tomography (SPECT) revealed no abnormalities other than a decreased cerebral blood flow (CBF) in the left striatum. After four courses of salvage chemotherapy, his clinical symptoms and asymmetric cerebral perfusion improved, suggesting that the decreased CBF had caused chorea. The significance of brain SPECT has not been fully clarified in patients with chorea-associated malignant lymphoma, warranting further investigations. Brain SPECT is an alternative approach to identify abnormalities in such patients.
en-copyright=
kn-copyright=

en-aut-name=KitamuraWataru
en-aut-sei=Kitamura
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EnnishiDaisuke
en-aut-sei=Ennishi
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YukawaRyoya
en-aut-sei=Yukawa
en-aut-mei=Ryoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshidaChikamasa
en-aut-sei=Yoshida
en-aut-mei=Chikamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakasukaHiroki
en-aut-sei=Takasuka
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujiwaraHideaki
en-aut-sei=Fujiwara
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsadaNoboru
en-aut-sei=Asada
en-aut-mei=Noboru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujiiKeiko
en-aut-sei=Fujii
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FujiiNobuharu
en-aut-sei=Fujii
en-aut-mei=Nobuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MatsuokaKen-Ichi
en-aut-sei=Matsuoka
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Hematology, Okayama City Hospital
kn-affil=

affil-num=6
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Division of Clinical Laboratory, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Division of Blood Transfusion, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=13
en-affil=Department of Neurology, Okayama University Hospital
kn-affil=

affil-num=14
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=
en-keyword=peripheral T-cell lymphoma
kn-keyword=peripheral T-cell lymphoma
en-keyword=chorea
kn-keyword=chorea
en-keyword=single photon-emission computed tomography
kn-keyword=single photon-emission computed tomography
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=16
article-no=
start-page=8689
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Glutathione and Related Molecules in Parkinsonism
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate cysteine readily becomes the oxidized dimeric cystine. Since neurons lack a cystine transport system, neuronal GSH synthesis depends on cystine uptake via the cystine/glutamate exchange transporter (xCT), GSH synthesis, and release in/from surrounding astrocytes. Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a detoxifying master transcription factor, is expressed mainly in astrocytes and activates the gene expression of various phase II drug-metabolizing enzymes or antioxidants including GSH-related molecules and metallothionein by binding to the antioxidant response element (ARE) of these genes. Accumulating evidence has shown the involvement of dysfunction of antioxidative molecules including GSH and its related molecules in the pathogenesis of Parkinson's disease (PD) or parkinsonian models. Furthermore, we found several agents targeting GSH synthesis in the astrocytes that protect nigrostriatal dopaminergic neuronal loss in PD models. In this article, the neuroprotective effects of supplementation and enhancement of GSH and its related molecules in PD pathology are reviewed, along with introducing new experimental findings, especially targeting of the xCT-GSH synthetic system and Nrf2-ARE pathway in astrocytes.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=glutathione
kn-keyword=glutathione
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=parkinsonism
kn-keyword=parkinsonism
en-keyword=astrocyte
kn-keyword=astrocyte
en-keyword=region specificity
kn-keyword=region specificity
en-keyword=striatum
kn-keyword=striatum
en-keyword=mesencephalon
kn-keyword=mesencephalon
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=Nrf2
kn-keyword=Nrf2
en-keyword=metallothionein
kn-keyword=metallothionein
en-keyword=serotonin 5-HT1A receptor
kn-keyword=serotonin 5-HT1A receptor
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=
article-no=
start-page=1511
end-page=1523
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=2021821
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neuroprotective Effects of Anti-high Mobility Group Box-1 Monoclonal Antibody Against Methamphetamine-Induced Dopaminergic Neurotoxicity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=High mobility group box-1 (HMGB1) is a ubiquitous non-histone nuclear protein that plays a key role as a transcriptional activator, with its extracellular release provoking inflammation. Inflammatory responses are essential in methamphetamine (METH)-induced acute dopaminergic neurotoxicity. In the present study, we examined the effects of neutralizing anti-HMGB1 monoclonal antibody (mAb) on METH-induced dopaminergic neurotoxicity in mice. BALB/c mice received a single intravenous administration of anti-HMGB1 mAb prior to intraperitoneal injections of METH (4 mg/kg x 2, at 2-h intervals). METH injections induced hyperthermia, an increase in plasma HMGB1 concentration, degeneration of dopaminergic nerve terminals, accumulation of microglia, and extracellular release of neuronal HMGB1 in the striatum. These METH-induced changes were significantly inhibited by intravenous administration of anti-HMGB1 mAb. In contrast, blood-brain barrier disruption occurred by METH injections was not suppressed. Our findings demonstrated the neuroprotective effects of anti-HMGB1 mAb against METH-induced dopaminergic neurotoxicity, suggesting that HMGB1 could play an initially important role in METH toxicity.
en-copyright=
kn-copyright=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurodaKeita
en-aut-sei=Kuroda
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IsookaNami
en-aut-sei=Isooka
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KikuokaRyo
en-aut-sei=Kikuoka
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinki
en-aut-sei=Murakami
en-aut-mei=Shinki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KamimaiSunao
en-aut-sei=Kamimai
en-aut-mei=Sunao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WangDengli
en-aut-sei=Wang
en-aut-mei=Dengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=LiuKeyue
en-aut-sei=Liu
en-aut-mei=Keyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=7
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=
kn-affil=

affil-num=11
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=methamphetamine
kn-keyword=methamphetamine
en-keyword=dopamine neuron
kn-keyword=dopamine neuron
en-keyword=high mobility group box-1
kn-keyword=high mobility group box-1
en-keyword=hyperthermia
kn-keyword=hyperthermia
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=neurotoxicity
kn-keyword=neurotoxicity
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=7
article-no=
start-page=789
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210707
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vagus Nerve Stimulation with Mild Stimulation Intensity Exerts Anti-Inflammatory and Neuroprotective Effects in Parkinson's Disease Model Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The major surgical treatment for Parkinson's disease (PD) is deep brain stimulation (DBS), but a less invasive treatment is desired. Vagus nerve stimulation (VNS) is a relatively safe treatment without cerebral invasiveness. In this study, we developed a wireless controllable electrical stimulator to examine the efficacy of VNS on PD model rats. Methods: Adult female Sprague-Dawley rats underwent placement of a cuff-type electrode and stimulator on the vagus nerve. Following which, 6-hydroxydopamine (6-OHDA) was administered into the left striatum to prepare a PD model. VNS was started immediately after 6-OHDA administration and continued for 14 days. We evaluated the therapeutic effects of VNS with behavioral and immunohistochemical outcome assays under different stimulation intensity (0.1, 0.25, 0.5 and 1 mA). Results: VNS with 0.25-0.5 mA intensity remarkably improved behavioral impairment, preserved dopamine neurons, reduced inflammatory glial cells, and increased noradrenergic neurons. On the other hand, VNS with 0.1 mA and 1 mA intensity did not display significant therapeutic efficacy. Conclusions: VNS with 0.25-0.5 mA intensity has anti-inflammatory and neuroprotective effects on PD model rats induced by 6-OHDA administration. In addition, we were able to confirm the practicality and effectiveness of the new experimental device.
en-copyright=
kn-copyright=

en-aut-name=KinIttetsu
en-aut-sei=Kin
en-aut-mei=Ittetsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KamedaMasahiro
en-aut-sei=Kameda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AgariTakashi
en-aut-sei=Agari
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkazakiMihoko
en-aut-sei=Okazaki
en-aut-mei=Mihoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HosomotoKakeru
en-aut-sei=Hosomoto
en-aut-mei=Kakeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KawauchiSatoshi
en-aut-sei=Kawauchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KuwaharaKen
en-aut-sei=Kuwahara
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MorimotoJun
en-aut-sei=Morimoto
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KinKyohei
en-aut-sei=Kin
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=UmakoshiMichiari
en-aut-sei=Umakoshi
en-aut-mei=Michiari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TomitaYousuke
en-aut-sei=Tomita
en-aut-mei=Yousuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TajiriNaoki
en-aut-sei=Tajiri
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=BorlonganCesario, V
en-aut-sei=Borlongan
en-aut-mei=Cesario, V
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Neurosurgery, Tokyo Metropolitan Neurological Hospital
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=

affil-num=16
en-affil=Department of Neurophysiology and Brain Science and Medical School, Graduate School of Medical Sciences and Medical School, Nagoya City University
kn-affil=

affil-num=17
en-affil=Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, 12901 Bruce B. Downs Blvd.
kn-affil=

affil-num=18
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=anti-inflammation
kn-keyword=anti-inflammation
en-keyword=less invasive therapy
kn-keyword=less invasive therapy
en-keyword=new experimental device
kn-keyword=new experimental device
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
en-keyword=vagus nerve stimulation
kn-keyword=vagus nerve stimulation
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=1
article-no=
start-page=8
end-page=12
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210330
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An Examination of mobile spinal cord stimulators on treating Parkinson disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In animal models of Parkinson disease (PD), spinal cord stimulation (SCS) exhibits neuroprotective effects. Recent advancements in SCS technology, most importantly mobile stimulators, allow for the conventional limitations of SCS such as limited stimulation time and restricted animal movements to be bypassed, offering potential avenues for improved clinical translation to PD patients. Small devices that could deliver continuous SCS to freely moving parkinsonian rats were shown to significantly improve behavior, preserve neurons and fibers in the substantia Nigra/striatum, reduce microglia infiltration, and increase laminin-positive area of the cerebral cortex. Through possible anti-inflammatory and angiogenic mechanisms, it has been demonstrated that there are behavioral and histological benefits to continuous SCS in a time-dependent manner. This review will discuss the benefits of this technology as well as focus on the limitations of current animal models.
en-copyright=
kn-copyright=

en-aut-name=WangZhen-Jie
en-aut-sei=Wang
en-aut-mei=Zhen-Jie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Neurosurgery and Brain Repair, Morsani College of Medicine, University of South Florida
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=6 hydroxydopamine
kn-keyword=6 hydroxydopamine
en-keyword=electrical stimulation
kn-keyword=electrical stimulation
en-keyword=neuroinflammation
kn-keyword=neuroinflammation
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=Parkinson disease
kn-keyword=Parkinson disease
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=3
article-no=
start-page=598
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190130
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Region-Specific Neuroprotective Features of Astrocytes against Oxidative Stress Induced by 6-Hydroxydopamine 
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In previous studies, we found regional differences in the induction of antioxidative molecules in astrocytes against oxidative stress, postulating that region-specific features of astrocytes lead region-specific vulnerability of neurons. We examined region-specific astrocytic features against dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) as an oxidative stress using co-culture of mesencephalic neurons and mesencephalic or striatal astrocytes in the present study. The 6-OHDA-induced reduction of mesencephalic dopamine neurons was inhibited by co-culturing with astrocytes. The co-culture of midbrain neurons with striatal astrocytes was more resistant to 6-OHDA than that with mesencephalic astrocytes. Furthermore, glia conditioned medium from 6-OHDA-treated striatal astrocytes showed a greater protective effect on the 6-OHDA-induced neurotoxicity and oxidative stress than that from mesencephalic astrocytes. The cDNA microarray analysis showed that the number of altered genes in both mesencephalic and striatal astrocytes was fewer than that changed in either astrocyte. The 6-OHDA treatment, apparently up-regulated expressions of Nrf2 and some anti-oxidative or Nrf2-regulating phase II, III detoxifying molecules related to glutathione synthesis and export in the striatal astrocytes but not mesencephalic astrocytes. There is a profound regional difference of gene expression in astrocytes induced by 6-OHDA. These results suggest that protective features of astrocytes against oxidative stress are more prominent in striatal astrocytes, possibly by secreting humoral factors in striatal astrocytes.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Okumura-TorigoeNao
en-aut-sei=Okumura-Torigoe
en-aut-mei=Nao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MurakamiShinki
en-aut-sei=Murakami
en-aut-mei=Shinki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medical, Dental and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Clinical Pharmacy, Okayama University Graduate School of Medical, Dental and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medical, Dental and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medical, Dental and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Clinical Pharmacy, Okayama University Graduate School of Medical, Dental and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Clinical Pharmacy, Okayama University Graduate School of Medical, Dental and Pharmaceutical Sciences
kn-affil=
en-keyword=astrocyte
kn-keyword=astrocyte
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=region-specificity
kn-keyword=region-specificity
en-keyword=striatum
kn-keyword=striatum
en-keyword=mesencephalon
kn-keyword=mesencephalon
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=6-hydroxydopamine
kn-keyword=6-hydroxydopamine
en-keyword=Nrf2
kn-keyword=Nrf2
en-keyword=phase II detoxifying molecules
kn-keyword=phase II detoxifying molecules
END

start-ver=1.4
cd-journal=joma
no-vol=30
cd-vols=
no-issue=4
article-no=
start-page=811
end-page=830
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200415
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Factors associated with development and distribution of granular/fuzzy astrocytes in neurodegenerative diseases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Granular/fuzzy astrocytes (GFAs), a subtype of “aging‐related tau astrogliopathy,” are noted in cases bearing various neurodegenerative diseases. However, the pathogenic significance of GFAs remains unclear. We immunohistochemically examined the frontal cortex, caudate nucleus, putamen and amygdala in 105 cases composed of argyrophilic grain disease cases (AGD, N = 26), and progressive supranuclear palsy (PSP, N = 10), Alzheimer’s disease (AD, N = 20) and primary age‐related tauopathy cases (PART, N = 18) lacking AGD, as well as 31 cases bearing other various neurodegenerative diseases to clarify (i) the distribution patterns of GFAs in AGD, and PSP, AD and PART lacking AGD, (ii) the impacts of major pathological factors and age on GFA formation and (iii) immunohistochemical features useful to understand the formation process of GFAs. In AGD cases, GFAs consistently occurred in the amygdala (100%), followed by the putamen (69.2%) and caudate nucleus and frontal cortex (57.7%, respectively). In PSP cases without AGD, GFAs were almost consistently noted in all regions examined (90–100%). In AD cases without AGD, GFAs were less frequent, developing preferably in the putamen (35.0%) and caudate nucleus (30.0%). PART cases without AGD had GFAs most frequently in the amygdala (35.3%), being more similar to AGD than to AD cases. Ordered logistic regression analyses using all cases demonstrated that the strongest independent factor of GFA formation in the frontal cortex and striatum was the diagnosis of PSP, while that in the amygdala was AGD. The age was not significantly associated with GFA formation in any region. In GFAs in AGD cases, phosphorylation and conformational change of tau, Gallyas‐positive glial threads indistinguishable from those in tufted astrocytes, and the activation of autophagy occurred sequentially. Given these findings, AGD, PSP, AD and PART cases may show distinct distributions of GFAs, which may provide clues to predict the underlying processes of primary tauopathies.
en-copyright=
kn-copyright=

en-aut-name=MikiTomoko
en-aut-sei=Miki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UenoShu‐ichi
en-aut-sei=Ueno
en-aut-mei=Shu‐ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakenoshitaShintaro
en-aut-sei=Takenoshita
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamadaNorihito
en-aut-sei=Yamada
en-aut-mei=Norihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurology, National Hospital Organization Minami‐Okayama Medical Center
kn-affil=

affil-num=4
en-affil=Department of Laboratory Medicine and Pathology, Zikei Institute of Psychiatry
kn-affil=

affil-num=5
en-affil=Dementia Research Project, Tokyo Metropolitan Institute of Medical Science
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=7
en-affil=Department of Neuropsychiatry, Ehime University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=aging‐related tau astrogliopathy
kn-keyword=aging‐related tau astrogliopathy
en-keyword=argyrophilic grain
kn-keyword=argyrophilic grain
en-keyword=granular/fuzzy astrocyte
kn-keyword=granular/fuzzy astrocyte
en-keyword=primary age‐related tauopathy
kn-keyword=primary age‐related tauopathy
en-keyword=tau
kn-keyword=tau
en-keyword=tufted astrocyte
kn-keyword=tufted astrocyte
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=164
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200616
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Long-Term Continuous Cervical Spinal Cord Stimulation Exerts Neuroprotective Effects in Experimental Parkinson's Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Spinal cord stimulation (SCS) exerts neuroprotective effects in animal models of Parkinson’s disease (PD). Conventional stimulation techniques entail limited stimulation time and restricted movement of animals, warranting the need for optimizing the SCS regimen to address the progressive nature of the disease and to improve its clinical translation to PD patients.</br>
Objective: Recognizing the limitations of conventional stimulation, we now investigated the effects of continuous SCS in freely moving parkinsonian rats.</br>
Methods: We developed a small device that could deliver continuous SCS. At the start of the experiment, thirty female Sprague-Dawley rats received the dopamine (DA)-depleting neurotoxin, 6-hydroxydopamine, into the right striatum. The SCS device was fixed below the shoulder area of the back of the animal, and a line from this device was passed under the skin to an electrode that was then implanted epidurally over the dorsal column. The rats were divided into three groups: control, 8-h stimulation, and 24-h stimulation, and behaviorally tested then euthanized for immunohistochemical analysis.</br>
Results: The 8- and 24-h stimulation groups displayed significant behavioral improvement compared to the control group. Both SCS-stimulated groups exhibited significantly preserved tyrosine hydroxylase (TH)-positive fibers and neurons in the striatum and substantia nigra pars compacta (SNc), respectively, compared to the control group. Notably, the 24-h stimulation group showed significantly pronounced preservation of the striatal TH-positive fibers compared to the 8-h stimulation group. Moreover, the 24-h group demonstrated significantly reduced number of microglia in the striatum and SNc and increased laminin-positive area of the cerebral cortex compared to the control group.</br>
Conclusions: This study demonstrated the behavioral and histological benefits of continuous SCS in a time-dependent manner in freely moving PD animals, possibly mediated by anti-inflammatory and angiogenic mechanisms.
en-copyright=
kn-copyright=

en-aut-name=KuwaharaKen
en-aut-sei=Kuwahara
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KamedaMasahiro
en-aut-sei=Kameda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HosomotoKakeru
en-aut-sei=Hosomoto
en-aut-mei=Kakeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinIttetsu
en-aut-sei=Kin
en-aut-mei=Ittetsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkazakiMihoko
en-aut-sei=Okazaki
en-aut-mei=Mihoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KawauchiSatoshi
en-aut-sei=Kawauchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TomitaYousuke
en-aut-sei=Tomita
en-aut-mei=Yousuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=UmakoshiMichiari
en-aut-sei=Umakoshi
en-aut-mei=Michiari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KinKyohei
en-aut-sei=Kin
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MorimotoJun
en-aut-sei=Morimoto
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=LeeJea-Young
en-aut-sei=Lee
en-aut-mei=Jea-Young
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TajiriNaoki
en-aut-sei=Tajiri
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=BorlonganCesar V.
en-aut-sei=Borlongan
en-aut-mei=Cesar V.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Neurosurgery and Brain Repair, Morsani College of Medicine, University of South Florida
kn-affil=

affil-num=16
en-affil=Department of Neurophysiology and Brain Science, Graduate School of Medical Sciences, Nagoya City University
kn-affil=

affil-num=17
en-affil=Department of Neurosurgery and Brain Repair, Morsani College of Medicine, University of South Florida
kn-affil=

affil-num=18
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=electrical stimulation
kn-keyword=electrical stimulation
en-keyword=neuroinflammation
kn-keyword=neuroinflammation
en-keyword=neuromodulation
kn-keyword=neuromodulation
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=6-hydroxydopamine
kn-keyword=6-hydroxydopamine
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=9
article-no=
start-page=3254
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Chronic Systemic Exposure to Low-Dose Rotenone Induced Central and Peripheral Neuropathology and Motor Deficits in Mice: Reproducible Animal Model of Parkinson's Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epidemiological studies demonstrated that pesticide exposure, such as rotenone and paraquat, increases the risk of Parkinson's disease (PD). Chronic systemic exposure to rotenone, a mitochondrial complex I inhibitor, could reproduce many features of PD. However, the adoption of the models is limiting because of variability in animal sensitivity and the inability of other investigators to consistently reproduce the PD neuropathology. In addition, most of rotenone models were produced in rats. Here, we tried to establish a high-reproducible rotenone model using C57BL/6J mice. The rotenone mouse model was produced by chronic systemic exposure to a low dose of rotenone (2.5 mg/kg/day) for 4 weeks by subcutaneous implantation of rotenone-filled osmotic mini pump. The rotenone-treated mice exhibited motor deficits assessed by open field, rotarod and cylinder test and gastrointestinal dysfunction. Rotenone treatment decreased the number of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) and lesioned nerve terminal in the striatum. In addition, we observed significant reduction of cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) and the intestinal myenteric plexus. Moreover, alpha-synuclein was accumulated in neuronal soma in the SNpc, DMV and intestinal myenteric plexus in rotenone-treated mice. These data suggest that the low-dose rotenone mouse model could reproduce behavioral and central and peripheral neurodegenerative features of PD and be a useful model for investigation of PD pathogenesis.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IsookaNami
en-aut-sei=Isooka
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImafukuFuminori
en-aut-sei=Imafuku
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SunJin
en-aut-sei=Sun
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KikuokaRyo
en-aut-sei=Kikuoka
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FurukawaChieko
en-aut-sei=Furukawa
en-aut-mei=Chieko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=rotenone
kn-keyword=rotenone
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
en-keyword=dopaminergic neuron
kn-keyword=dopaminergic neuron
en-keyword=dorsal motor nucleus of the vagus
kn-keyword=dorsal motor nucleus of the vagus
en-keyword=myenteric plexus
kn-keyword=myenteric plexus
en-keyword=neurodegeneration
kn-keyword=neurodegeneration
en-keyword=α-synuclein
kn-keyword=α-synuclein
en-keyword=motor deficit
kn-keyword=motor deficit
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=1
article-no=
start-page=10956
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190729
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In vivo direct reprogramming of glial linage to mature neurons after cerebral ischemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The therapeutic effect of in vivo direct reprogramming on ischemic stroke has not been evaluated. In the present study, a retroviral solution (1.5-2.0 × 107 /ul) of mock pMX-GFP (n = 13) or pMX-Ascl1/Sox2/NeuroD1 (ASN) (n = 14) was directly injected into the ipsilateral striatum and cortex 3 days after 30 min of transient cerebral ischemia. The reprogrammed cells first expressed neuronal progenitor marker Dcx 7 and 21 days after viral injection, then expressed mature neuronal marker NeuN. This was accompanied by morphological changes, including long processes and synapse-like structures, 49 days after viral injection. Meanwhile, therapeutic improvement was not detected both in clinical scores or infarct volume. The present study provides a future novel self-repair strategy for ischemic stroke with beneficial modifications of the inducer-suppressor balance.
en-copyright=
kn-copyright=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatoKota
en-aut-sei=Sato
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=4
article-no=
start-page=285
end-page=297
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dynamic Reorganization of Microtubule and Glioma Invasion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Gliomas are characterized as highly diffuse infiltrating tumors, and currently available treatments such as surgery, radiation and chemotherapy are unfeasible or show limited efficacy against these tumors. Recent genetic and epigenetic analyses of glioma have revealed increasing evidence of the role of driver genetic alterations in glioma development and led to the identification of prognostic factors. Despite these findings, the survival rates of glioma patients remain low, and alternative treatments and novel targets are needed. Recent studies identified neural stem cells as the possible origin of gliomas, and some evidence has revealed shared functions and mechanisms between glioma cells and neurons, also supporting their similarity. The cytoskeleton plays important roles in the migration of normal cells as well as cancer cells. Recent reports have described a role for microtubules, a component of the cytoskeleton, in glioma invasion. Notably, several factors that regulate microtubule functions, such as microtubule-associated proteins, plus-end tracking proteins, or motor proteins, are upregulated in glioma tissues compared with normal tissue, and upregulation of these factors is associated with high invasiveness of glioma cells. In this review, we describe the mechanism of microtubules in glioma invasion and discuss the possibility of microtubule-targeted therapy to inhibit glioma invasion.
en-copyright=
kn-copyright=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IchikawaTomotsugu
en-aut-sei=Ichikawa
en-aut-mei=Tomotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurozumiKazuhiko
en-aut-sei=Kurozumi
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Neurosurgery, The University of Texas Health Science Center at Houston
kn-affil=

affil-num=2
en-affil=Department of Neurosurgery, Kagawa Prefectural Central Hospital
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=glioma
kn-keyword=glioma
en-keyword=cytoskeletons
kn-keyword=cytoskeletons
en-keyword=invasion
kn-keyword=invasion
en-keyword=microtubules
kn-keyword=microtubules
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=6
article-no=
start-page=e65983
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Transplantation of melanocytes obtained from the skin ameliorates apomorphine-induced abnormal behavior in rodent hemi-parkinsonian models
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tyrosinase, which catalyzes both the hydroxylation of tyrosine and consequent oxidation of L-DOPA to form melanin in melanocytes, is also expressed in the brain, and oxidizes L-DOPA and dopamine. Replacement of dopamine synthesis by tyrosinase was reported in tyrosine hydroxylase null mice. To examine the potential benefits of autograft cell transplantation for patients with Parkinson's disease, tyrosinase-producing cells including melanocytes, were transplanted into the striatum of hemi-parkinsonian model rats or mice lesioned with 6-hydroxydopamine. Marked improvement in apomorphine-induced rotation was noted at day 40 after intrastriatal melanoma cell transplantation. Transplantation of tyrosinase cDNA-transfected hepatoma cells, which constitutively produce L-DOPA, resulted in marked amelioration of the asymmetric apomorphine-induced rotation in hemi-parkinsonian mice and the effect was present up to 2 months. Moreover, parkinsonian mice transplanted with melanocytes from the back skin of black newborn mice, but not from albino mice, showed marked improvement in the apomorphine-induced rotation behavior up to 3 months after the transplantation. Dopamine-positive signals were seen around the surviving transplants in these experiments. Taken together with previous studies showing dopamine synthesis and metabolism by tyrosinase, these results highlight therapeutic potential of intrastriatal autograft cell transplantation of melanocytes in patients with Parkinson's disease.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Francisco J.Diaz-Corrales
en-aut-sei=Francisco J.
en-aut-mei=Diaz-Corrales
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HigashiYouichirou
en-aut-sei=Higashi
en-aut-mei=Youichirou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NambaMasayoshi
en-aut-sei=Namba
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OgawaNorio
en-aut-sei=Ogawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Brain Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=3
article-no=
start-page=285
end-page=298
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neuroprotective Effects of Metallothionein Against Rotenone-Induced Myenteric Neurodegeneration in Parkinsonian Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Parkinson's disease (PD) is a neurodegenerative disease with motor symptoms as well as non-motor symptoms that precede the onset of motor symptoms. Mitochondrial complex I inhibitor, rotenone, has been widely used to reproduce PD pathology in the central nervous system (CNS) and enteric nervous system (ENS). We reported previously that metallothioneins (MTs) released from astrocytes can protect dopaminergic neurons against oxidative stress. The present study examined the changes in MT expression by chronic systemic rotenone administration in the striatum and colonic myenteric plexus of C57BL mice. In addition, we investigated the effects of MT depletion on rotenone-induced neurodegeneration in CNS and ENS using MT-1 and MT-2 knockout (MT KO) mice, or using primary cultured neurons from MT KO mice. In normal C57BL mice, subcutaneous administration of rotenone for 6 weeks caused neurodegeneration, increased MT expression with astrocytes activation in the striatum and myenteric plexus. MT KO mice showed more severe myenteric neuronal damage by rotenone administration after 4 weeks than wild-type mice, accompanied by reduced astroglial activation. In primary cultured mesencephalic neurons from MT KO mice, rotenone exposure induced neurotoxicity in dopaminergic neurons, which was complemented by addition of recombinant protein. The present results suggest that MT seems to provide protection against neurodegeneration in ENS of rotenone-induced PD model mice.
en-copyright=
kn-copyright=

en-aut-name=MurakamiShinki
en-aut-sei=Murakami
en-aut-mei=Shinki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SogawaNorio
en-aut-sei=Sogawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyoshiKo
en-aut-sei=Miyoshi
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Brain Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Brain Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Dent Pharmacol

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Brain Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Brain Sci
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
en-keyword=Rotenone
kn-keyword=Rotenone
en-keyword=Enteric nervous system
kn-keyword=Enteric nervous system
en-keyword=Astrocytes
kn-keyword=Astrocytes
en-keyword=Metallothionein
kn-keyword=Metallothionein
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=3
article-no=
start-page=203
end-page=208
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20141201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Modulation of neuronal function and neuroprotection by astrocytes
kn-title=アストロサイトによる神経機能修飾とパーキンソン病での神経保護
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=浅沼幹人
kn-aut-sei=浅沼
kn-aut-mei=幹人
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　神経ゲノム学
en-keyword=アストロサイト
kn-keyword=アストロサイト
en-keyword=抗酸化防御機構
kn-keyword=抗酸化防御機構
en-keyword=パーキンソン病
kn-keyword=パーキンソン病
en-keyword=メタロチオネイン
kn-keyword=メタロチオネイン
en-keyword=Nrf2
kn-keyword=Nrf2
END

start-ver=1.4
cd-journal=joma
no-vol=1502
cd-vols=
no-issue=
article-no=
start-page=55
end-page=70
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130328
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The neuroprotective and neurorescue effects of carbamylated erythropoietin Fc fusion protein (CEPO-Fc) in a rat model of Parkinson's disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Parkinson's disease is characterized by progressive degeneration of dopaminergic neurons. Thus the development of therapeutic neuroprotection and neurorescue strategies to mitigate disease progression is important. In this study we evaluated the neuroprotective/rescue effects of erythropoietin Fc fusion protein (EPO-Fc) and carbamylated erythropoietin Fe fusion protein (CEPO-Fc) in a rat model of Parkinson's disease. Adult female Sprague-Dawley rats received intraperitoneal injection of EPO-Fc, CEPO-Fc or PBS. Behavioral evaluations consisted of rota-rod, cylinder and amphetamine-induced rotation tests. In the neuroprotection experiment, the CEPO-Fc group demonstrated significant improvement compared with the EPO-Fc group on the amphetamine-induced rotation test throughout the four-week follow-up period. Histologically, significantly more tyrosine hydroxylase (TH)-positive neurons were recognized in the substantia nigra (SN) pars compacta in the CEPO-Fc group than in the PBS and EPO-Fc groups. In the neurorescue experiment, rats receiving CEPO-Fc showed significantly better behavioural scores than those receiving PBS. The histological data concerning striatum also showed that the CEPO-Fc group had significantly better preservation of TH-positive fibers compared to the PBS and EPO-Fc groups. Importantly, there were no increases in hematocrit or hemoglobin levels in the CEPO-Fc group in either the neuroprotection or the neurorescue experiments. In conclusion, the newly developed CEPO-Fc might confer neuroprotective and neurorescue benefits in a rat model of Parkinson's disease without the side effects associated with polycythemia. CEPO-Fc might be a therapeutic tool for patients with Parkinson's disease.
en-copyright=
kn-copyright=

en-aut-name=TayraJudith Thomas
en-aut-sei=Tayra
en-aut-mei=Judith Thomas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KamedaMasahiro
en-aut-sei=Kameda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AgariTakashi
en-aut-sei=Agari
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KadotaTomohito
en-aut-sei=Kadota
en-aut-mei=Tomohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WangFeifei
en-aut-sei=Wang
en-aut-mei=Feifei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KikuchiYoichiro
en-aut-sei=Kikuchi
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=LiangHanbai
en-aut-sei=Liang
en-aut-mei=Hanbai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShinkoAiko
en-aut-sei=Shinko
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WakamoriTakaaki
en-aut-sei=Wakamori
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=VcelarBrigitta
en-aut-sei=Vcelar
en-aut-mei=Brigitta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WeikRobert
en-aut-sei=Weik
en-aut-mei=Robert
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg

affil-num=11
en-affil=
kn-affil=Polymun Sci GmbH

affil-num=12
en-affil=
kn-affil=Polymun Sci GmbH

affil-num=13
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Neurol Surg
en-keyword=Carbamylated erythropoietin
kn-keyword=Carbamylated erythropoietin
en-keyword=Dopamine
kn-keyword=Dopamine
en-keyword=Neuroprotection
kn-keyword=Neuroprotection
en-keyword=Neurorescue
kn-keyword=Neurorescue
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=439
article-no=
start-page=878
end-page=904
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1926
dt-pub=19260831
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Ueber die Verbindung der Hirnrinde mit dem Corpus striatum und Globus pallidus beim Kaninchen
kn-title=家兎ノ大腦皮質ト線状體竝ニ淡蒼球トノ間ノ神經纎維ノ連結ニ就テ
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Versuch I. Nach Auskratzung des fast ganzen Areals des rechten Frontallappens beim Kaninchen uatersuchte ich mit Hilfe der Marchischen Methode die Frontalschnitte des Gehirns. Im Stratum subcallosum sowie in der dorsalen Partie des Stratum zonale nuclei caudati, der Capsula interna u. des Putamens sieht man überall feine Degenerationsfasern mit Ausnahme ihren caudalen u. oralen Enden. Die im Globus pallidus befindlichen Degenerationsfasern verschieben sich allmahlich nach medianwärts, je weiter man sie caudalwarts verfolgt. In die Substautia nigra treten zahlreiche jiemlich dicke Degenerationsfasern vom Hirnschenkelfuss ein, um sich hauptsachlich in ihrem medialen Teil zu verbreiten. Am caudalen Ende der Substantia nigra sind diese Degenerationsfasern stark vermindert.
Versuch II. Bei diesem Fall wurde das Tier genau wie oben operiert, um die Nisslsche Degeneration zu untersuchen. Keine Veranderung der Ganglienzellen liess sich im Nucleus caudatus, Putamen, Globus pallidus u. in der Substantia nigra nachweisen, wohl aber eine Gliawucherung im oralen u. mittleren Teil des Nucleus caudatus, Putamen, Stratum subcallosum, Stratum zonale n. c., der Capsula interna und externa. Diese Gliawucherung scheint mir auf dem Reiz zuberuhen, welcher durch die Zerfallung der Markfasern veranlasst wurde. Versuch III. Nach Zerstörung des Nucleus caudatus u. Putamens konnte man gar keine Degenerationsfasern in der Grosshirnrinde besonders des Frontallappens finden. Versuch IV. In dorsoventraler Richtung wurde das Kopf des rechten Nucleus caudatus geschnitten u. die Untersuchung erfolgte nach der Nisslschen Methode. Die Ganglienpartie, welche auf der medialen Seite der Schnittlinie liegt, fällt einer hochgradigen Degeneration anheim, so dass die meisten Ganglienzellen spurlos verschwunden und sparlich übrigbleibende stark degeneriert sind. Trotzdem ist keine Gliawucherung zu sehen. Auf der lateralen Seite der Schnittlinie trifft man keine Degeneration der Ganglienzellen, wohl aber eine massige Vermehrung der Gliazellen, welche die Wunde entlang stattfindet. Versuch V.
Ich zerstörte die dorsale Partie des Kopfes des Nucleus caudatus, wobei der dorsale Teil der Capsula interna mitbeschadigt wurde. Bei diesem Fall lasst sich keine Marchi-Degeneration im Putamen nachweisen. So halte ich es für sehr zweiferhaft, ob Fasern, welche nach Wilson den Nucleus caudatus mit dem Putamen verbinden sollen wirklich vorhnaden sind. Schluss. 1. Ein Teil der zentrifugalen Nervenfasern, die aus dem Frontallappen entspringen verbreitet sich u. endigt in der dorsalen Partie des Nucleus caudatus auf dem Wege des Stratum subcallosum. 2. Ein anderer Teil dieser zentrifugalen Fasern tritt ebenfalls durch Vermittelung des Stratum subcallosum in das Stratum zonale n. c. ein, um an der dorsalen Oberfläche des Nucleus caudatus zu endigen. 3. Ein dritter Teil der zentrigfualen Nervenfasern, welch aus dem Frontallappen entspringen, begiebt sich durch die Corona radiata hindurch nach der Capsula externa, wovon er ins Putamen u. z. hauptsachlich in seine dorsale Partie ausstrahlt. 4. Ein vierter Teil der zentrifugalen Nervenfasern, die dem Frontallappen entstammen, zieht durch die Capsula interna und die mediale Partie des Globus pallidus hindurch weiter caudalwarts. Ob diese Fasern zum Teil im Globus pallidus endigen, ist nicht mit Sicherheit zu entscheiden. 5. Es gibt keine zentripetalen Fasern, welche aus dem Corpus striatum u. Globus pallidus entspringend nach dem Frontallappen ziehen. 6. Die Nervenfasern innerhalb des Nucleus caudatus verlaufen in mediolateraler Richtung. 7. Solche Fasern, wie den vom Nucleus caudatns nach dem Putamen ziehenden lassen sich nicht nachweisen.
en-copyright=
kn-copyright=

en-aut-name=InuiSaburo
en-aut-sei=Inui
en-aut-mei=Saburo
kn-aut-name=乾三郎
kn-aut-sei=乾
kn-aut-mei=三郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=447
article-no=
start-page=455
end-page=478
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1927
dt-pub=19270430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Ueber die Verbindung des Globus pallidus mit dem Corpus Luysi und der Substantia nigra beim Kaninchen
kn-title=家兎ノ淡蒼球トLuys氏體竝ニ黒質間ノ神經纖維ノ連結ニ就テ
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Versuch 1. Ich zerstörte das hintere Ende des rechten Globus pallidus beim Kaninchen mit einem nadelförmigen Instrument durch die Hirnrinde hindurch. 21 Tage nach der Operation wurde das Tier durch Verblutung getötet und eine Serie der Frontalschnitte des Gehirns nach Marchi untersucht. Der Nucleus caudatus der operierten Seite enthält feine spärliche Degenerationsfasern divergierend ins Putamen ein. Daneben sieht man zahlreiche feine Degenerationsfasern im rechten Corpus Luysì und im hinteren lateralen Teil der rechten Substantia nigra. Sie kommen vom Globus palidus durch den Pes pedunculi dazu. A ch in der Substantia nigra der nicht operierten Seite sind spärliche Degenerationsfasern mit Sicherheit vorhanden, während der Globus pallidus und das Corpus Luysi auf der linken Seite von ihnen ganz frei zu sein scheinen. Versuch 2. Die Operation und Untersuchung wurden beim Kaninchen genau wie oben ausgeführt. Doch bei diesem Fall ist die Läsion im rechten Globus pallidus etwas kleiner und liegt etwas weiter vorn als bei dem vorigen. Die Degenerationsfasern im Nucleus caudatus, Putamen und Corpus Luysi zeigen ganz ähnliches Verhältnis wie im voringen Fall, wenn auch ibre Zahl im Putamen und Corpus Luysi viel spärlicher ist. Im Gegensatz zum ersten Fall strahlen sich die Degenerationsfasern hauptsächlich in den medialen und mittleren Teil der Substantia nigra aus. Man vermisst Degenerationsfasern im Nucleus caudatus, Putamen, Globus pallidus und Corpus Luysi der anderen Seite, dagegen finden sich die zahlreichen dicken Degenerationsfasern im hinteren Teil der linken Substantia nigra. Ueber die Ganglienzellen des Globus pallìdus beim Kaninchen. Nach Bielschowsky, welchem wir eine genaue struktuelle Kenntnis des Globus pallidus verdanken, enthält der Glubus pallidus beim Menschen nur einen einzigen Ganglienzelltypus. Die Zellen sollen bald polygonal bald pyramiden- oder spinderförmig sein, die stark chromatophylen Nisslschollen grob und parallel zur Längsachse des Zellkörpers geordnet. Auch die Dendriten, welche hauptsächlich aus dem Spindelpol der Zellen entspringen, enthalten die Nisslschollen eine Strecke weit. Der grosse und bläschenartige Kern liegt immer in der Mitte der Längsachse des Zellkörpers. Beim Kaninchen jedoch sind die Zellen des Globus pallidus keinesweges gleichmässig in Bezug auf ihre Grösse und Anordnung, so dass ich an der a d der Nisslschen Präparate von ihnen folgende 3 Arten unterscheiden kann. 1. Grosse Zellen, welche sich nicht im oralen Teil des Globus pallidus, sondern in den mittleren und caudalen Abschnitte desselben finden. Sie sind etwas grösser als die grossen Zellen des Corpus striatum und an der Peripherie, besonders im ventralen und lateralen Teil des Globus pallidus lokalisiert. In der mittleren Schnittebene des Ganglions finden sie sich aber vorwiegend in seinem ventralen Teil, wo sie eine dichte Zellengruppe bilden. Was ihre Gestalt und Struktur betrifft, so gilt die Angabe von Bielschowsky. 2. Mittelgrosse Zellen, welche ziemlich gleic mässig in allen Abschnitten des Globus pallidus zerstreut vorhanden sind, nur dass in der Ebene, wo die grossen Zellen vorliegen, hauptsächlich in der Mitte des Globus pallidus. Ihnen gehören die meisten Nervenzellen des Grobus pallidus an. Sie haben dieserbe Struktur wie die genanten grossen Zellen, und gleichen an Grösse fast den grossen Zellen des Corpus stristum. 3. Kleine Zellen, welche wenn auch viel spärlicher doch ebenfalls überall im Globus pallidus vorhanden sind. Die Mehrzahl von ihnen hat die gleiche Form, wie Bielschowsky angiebt, während einigen wenige verglichen mit den der kleinen Zellen des Corpus striatum, mehr kuglich sind. An Grösse sind sie fast gleich den kleinen Zellen des Corpus striatum. Versuch 3. Nachdem der hintere Ted der rechten Substantia nigra beim Kaninchen durch die Hirnrinde hindurch mit einer Nadel zerstört worden war untersuchte ich mit Hilfe der Nisslschen Methode die Frontalschnitte des betreffenden Gebirns. Keine Veränderung der Ganglienzellen lässt sich im Nucleus caudatus und Putamen nachweisen, wohl aber eine Anzahl Ganglienzellen im rechten Globus pallidus fallen der Degeneration anheim, indem sie eine Chromatolysenerscheinung mit eider leichten Aufblähung des Zellkörpers und eider peripheren Verschiebung des Kerns zeigen. Auch im Globus pallidus der gegenüberliegenden Seite aieht man spärliche Ganglierizellen, welche ebenfalls die Nissidegeneration aufweisen. Ich zerstörte den hinteren Teil des linken Corpus Luysi durch die Hirnrindc hindurch beim Kaninchen, um die Nissldegeneration der Ganglien des extrapyramidalen Nervensystems an der Hand der Frontalserien-schnitte zu untersuchen. In den beiderseitigen Substantiae nigrae findet sich keine Degeneration der Gangliepzellen. Eine Anzahl Ganglienzellen im Globus pallidus zeigen auf beiden Seite die leichtgradige Degeneration, welche sich wie im vorigen Falle durch eine Aufösung der Nisllschollen mit leichter Aufblähung des Zellkörpers und eine peripherische Verlagerung des undeutlich begrenzten Kerns, oder öfters durch die Verschwommenheit des Kemkörperchens auszeichnet. Diese Degenerationserscheinungen sind hauptsächlich in den grossen Zellen meines 1. Typus des Globus pallidus zu sehen, wärend sie in den mittelgrossen und kleigen Zellen desselben nur selten beobachtet werden. Im Corpus striatum lässt sich keine Degeneration der Ganglienzellen nachweisen. Schluss. 1. Es gibt die Fasern, welche vom Globus pallidus entspringend nach dem Putamen ziehen. 2. Die Fasern, welche vom Globus pallidus nach dem Nucleus caudatus ziehen, lassen sich nachweisen. 3. Die Fasern, welche sich vom Globus pallidus nach dem Corpus Luysi begeben, entspringen hauptsächlich aus dem caudalen Teil des ersteren. 4. Die aus dem mittleren Teil des Globus pallidus entspringenden Fasern strahlen sich hauptsächlich in die mediale und mittlere Partie der Substantia nigra aps u. z. auf derselben Seite, wärend die Fasern aus dem caudalen Teil des Globus pallidus sich in die laterale Partie der gleichseitigen Substantia nigra ausstrahlen. 5. Der Globus pallidus steht in Verbindung sowohl mit der gleichseitigen wie auch mit der anderseitigen Substantia nigra. 6. Es giebt keine Kommissurenfasern zwischen den beiderseitigen Globi pallidi.
en-copyright=
kn-copyright=

en-aut-name=InuiSaburo
en-aut-sei=Inui
en-aut-mei=Saburo
kn-aut-name=乾三郎
kn-aut-sei=乾
kn-aut-mei=三郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室
END

start-ver=1.4
cd-journal=joma
no-vol=40
cd-vols=
no-issue=9
article-no=
start-page=1958
end-page=1966
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1928
dt-pub=19280930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Über die Verbindung des Corpus Luysi mit dem Globus pallidus und dem Corpus striatum, sowie über die Kommissurenfasern zwischen beiderseitigen Corpora Luysi
kn-title=Luys氏體ヨリ、淡蒼球及ビ線状體ニ至ル纖維竝ニ兩側Luys氏體間ノ連結ニ就テ
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Die aus dem Corpus Luysi entspringend nach dem Globus pallidus und dem Corpus striatum ziehenden Fasern sind von einigen Autoren schon angegeben werden, aber es gibt keine Arbeit, welche diese Tatsache auf Grund der Nisslschen Methode bestätigt. Dazu kommt noch, dass die Frage offen bleibt, auf welchem Wege sich die betreffenden Fasern nach dem Linsenkern und dem Nucleus caudatus begeben. Dasselbe gibt auch für die Frage, auf welche Weise die beiderseitigen Corpora Luysi verbunden sind. Einige Autoren balten die Forelsche Kreuzung für diese Verbindungsbahn, andere die Ansicht vertreten, dass die Commissura supramamillaris daran beteiligt ist Nach einer dritten Ansicht findet die betreffende Verbindung via Commissura Meynerti statt. Um diese Frage zn entscheiden, habe ich einige Versuche an Kaninchen angestellt. Die aus der Läsionsstelle des Corpus Luysi entstammenden degenerierten Fasern schlagen zwei verschiedene Richtungen ein; eine Anzahl von ihnen zieht nach kranialwärts und passiert durch den Hirnschenkelfuss, um dann in der Linsenkernschlinge weiter kranio-lateralwärts schreitend sich schliesslich im Globus pallidus und im Putamen zu zersplittern, während die übrigen Fasern zum grössten Teile medio-kaudalwärts in die Forelsche Kreuzung, zum kleinen Teile aber in die Commissura supramamillaris eintreten, um im Corpus Luysi der entgegengesetzten Seite zu endigen. Nach Zerstörung des Globus pallidus oder des Putamens sieht man einige degenerierte Zellen im Corpus Luysi auf der operierten Seite, indem sie leicht aufgebläht sind und manchmal keine Kerne nachweisen lassen. Daraus kann man schliessen, dass die aus dem Corpus Luysi entspringenden Fasern sich in die Linsenkernschlinge mischen, nachdem sie den Hirnschenkelfuss durchbohrt haben, und schliesslich im Globus palldus und Putamen endigen. Dagegen kann ich nicht sicher Fasern ermitteln, welche aus dem Corpus Luysi entspringend nach dem Nucleus caudatus ziehen. Die beiderseitigen Corpora Luysi verbinden sich hauptsächlich durch die Forelsche Kreuzung, zum kleinen Teile aber auch durch die Commissura supramamillaris.
en-copyright=
kn-copyright=

en-aut-name=InuiSaburo
en-aut-sei=Inui
en-aut-mei=Saburo
kn-aut-name=乾三郎
kn-aut-sei=乾
kn-aut-mei=三郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室
END

start-ver=1.4
cd-journal=joma
no-vol=41
cd-vols=
no-issue=12
article-no=
start-page=2808
end-page=2866
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1929
dt-pub=19291231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Experimentelle Studie über die Faserverbindung der Grosshirnrinde des Kaninchens
kn-title=大腦皮質纖維結合ニ關スル實驗的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Auf Grund der Marchi-Serien von 15 Kaninchenhirnen versucht Verf. die intra-, inter- und extrakortikalen Verbindungen näher zu bestimmen. Die Ergebnisse sind folgende. I. Die Assoziationsfaser. 1. Diese Fasern setzen kortikale Felder in Verbindung, wobei man deutlich 3 Systeme, nämlich die intrakortikale Querfaserschicht, das superfizielle Marklager und das Balkenlängsbündel, erkennt. 2. Die intrakortikale Querfaserschicht ist der kürzeste Weg, der die inneren Haupt-schichten der benachbarten Rindenanteile miteinander verbindet. Die einzige Ausnahme bilden nur Areae limbica et retrosplenialis, wo die Fasern durch die äusseren Schichten ziehen. 3. Das superfizielle Marklager und das Balkenlängsbündel bestehen aus Fasern von verschiedener Länge, deren Ursprungs- und Endstätten auch in den inneren Zonen der Rinde niedergelegt sind. 4. Das Stratum subcallosum verbindet den Zentral-, Parietal- und Schläfenlappen untereinander und wiederum den jeden einzelnen mit dem Striatum. 5. Zwischen dem Frontal- und Occipitalhirne existiert keine direkte Verbin-dungsbrücke. II. Die Kommissurfaser. 1. Der Hauptteil der Fasern, der sich als das Balkensystem darstellt, zeigt bestimmte lokalisatorische Verhältnisse. Die aus den frontalen sowie zentralen Gebieten kommenden Fasern ziehen durch das Knie des Balkens, die dem Parietallappen entstammenden durch dessen mittlere Partie, und die aus den occipitotemporalen Hirnen sind im Splenium verteilt. Dabei bilden Züge aus mehr medialen Rindenanteilen immer das oberflächlicher liegende Faserlager, die aus mehr lateralen Gegenden daher das tiefere. 2. Ein kleiner Teil der Kommissurfasern verläuft durch die Capsula externa und Commissura anterior. III. Die Projektionsfaser. 1. Die Capsula interna repräsentiert den Hauptzug der Projektionsfasern; ein kleiner Teil solcher aus den medialen Teilen der Areae limbica et retrosplenialis geht in Fornix longus hinein. 2. Im Mark der Rinde lassen sich 2 Faserlager, nämlich das oberflächliche und das das tiefe, unterscheiden. Das erstere tritt immer mit den naheliegenden subkortikalen Zentren wie den Thalamuskernen in Verbindung. Aus den letzteren kommen nur die langen Projektionszüge heraus, wie die Pyramiden-, kortikobulbäre, kortikopontine Bahn usw. 3. Aus den Einzelheiten solcher Verbindungen sind die folgenden Punkte besonders hervorzuheben. a. Direkter Zusammenhang besteht zwischen dem Striatum einerseits, den unteren parietalen Feldern, dem vorderen, unteren Teile des Temporalhirns und dem ganzen Areal des Zentrallappens andererseits. Das frontale Gebiet hat dagegen keinerlei Verbindung mit dem Striatum. b. Zwischen dem Pallidum und der Area retrosplenialis ist eine Verbindung nach-gewiesen. c. Die Verbindung zwischen dem Thalamus und der Rinde ist eine hochkomplizierte. Der mediale Kern steht nämlich mit den frontozentralen Gebieten in Verbindung; der laterale Kern mit der Area retrosplenialis, dem Parietal-, Occipital- und Temporallappen sowie den Zentralgebieten (1+3); der Ventralkern wieder mit den Zentralgebieten und dem Temporallappen; die Zona reticularis mit der Area retrosplenialis, der Parietal- und Temporalrinde. d. Der äussere Kniehöcker und der vordere Vierhügel haben Verbindungen mit dem Occipitalhirne nebst dessen anliegenden Gegenden, nämlich dem Parietal-, Temporal-lappen und der Area retrosplenialis. e. Der innere Kniehöcker ist verbunden mit dem Temporallappen und dem unteren Teile der Parietalrinde. f. Der Luyssche Körper hat eine Verbindung mit der Area retrosplenialis.
g. Der Mamillarkörper ist mit den Areae limbica et retrosplenialis über 2 Wege verbunden, von denen einer der Tractus corticomamillaris der Autoren, der andere der Tractus corticothalamomamillaris mihi ist. h. Die Substantia nigra hat Verbindungen mit dem Frontallappen, den zentralen Gebieten, der Parietalrinde und dem vorderen Teile des Parietalhirns. i. Die Pyramidenbahn nimmt ihren Ursprung hauptsächlich in der Area 4, einiger-massen auch noch in den Areas 1+3. j. Die Kortikobulbäre Bahn stammt aus der vorderen Partie der Area 4. k. Ausser den vielfach beschriebenen fronto-, temporo-, occipitopontinen Bahenen
existiert noch ein mächtiger Brückenfaserzug aus der Area retrosplenialis.
en-copyright=
kn-copyright=

en-aut-name=OkumaTaiji
en-aut-sei=Okuma
en-aut-mei=Taiji
kn-aut-name=大熊泰治
kn-aut-sei=大熊
kn-aut-mei=泰治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學精神病學教室
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=2
article-no=
start-page=403
end-page=429
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1930
dt-pub=19300228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Beiträge zum Parkinsonismus
kn-title=「パルキンソニスムス」症例補遺
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ich habe eine Gelegenheit gehabt, bei der drei Fällen von Parkinsonismus die klinischen Symptome, Leberfunktion sowie das Verhalten des vegetativen Nervensystems zu untersuchen, und die nachfolgende Resultate erzielt worden ist. 1. Unter denen sind 2 Fälle postencephalitische Natur und ein Fall Paralysis agitans gewesen. Der Parkinsonismus postencephalitischer Natur war dem Paralysis agitans sine agitatione sehr ähnlich. Es ist aber bemerkenswertig, dass unter den ersten 2 Fällen der eine mit der myastenischer Erscheinung begleitet war und der andere erst nach dem Verlauf des 8 Monate lang anhaltenden, hartnäckigen Singultus epidemicus begann, der sich an das akute Stadium der encephalitis epidemica eingestellt hatte. Bei dem Fall Paralysis agitans handelt es sich um eine 36 jährige Frau, die erst im 29 Lebensjahre davon befallen war. Im allgemeinen beginnt diese Krankheit erst im höheren Lebensalter und äussert sich vor allem mit dem Zittern an den oberen Extremitäten, aber diese Patientin ist damit mehr früheren Alter befallen worden und begann das Zittern zuerst am linken Bein anzutreffen, sodann allmählich andere Körperteile wie die folgende Reihe affiziert worden waren: rechte Bein, linke uud rechte Oberextremitäten. 2. Was die Leberfunktionsprüfungen anbelangt, so wurde sie mit den verschiedenen Methoden ausgeführt und wenn auch die Ergebnisse am sämtlichen Fällen ganz exakt nicht übereinander stimmt, sondern findet es miteinander einige Abweichungen, aber möchte ich im grossen Züge schliessen, dass bei jeden Fällen irgendeine Störung der Leberfunktion vorliege und ich stimme der Meinung von Lewy und Dresel zu, der die Leberfunktionsstörung bei dem postencephalitischen Parkinsonismus auf eine pathologische Veränderung des im Striatum vorhandenen Zentrums des vegetativen Nervensystems zurückgeführt. 3. Was das vegetativen Nervensystem anbelangt, so findet man bei dem Parkinsonismus immer den Erregungszustand des ganzen System und habe ich erkannt, dass sowohl Muskelrigidität als auch Zittern bei Parkinsonismus durch die Steigerung des sympathischen- und parasympathischen Tonus zustande kommt, wie von Kure, Araki, Schibata und Inoue etc. betont wurde.
en-copyright=
kn-copyright=

en-aut-name=TsujiKaneji
en-aut-sei=Tsuji
en-aut-mei=Kaneji
kn-aut-name=辻鹿子治
kn-aut-sei=辻
kn-aut-mei=鹿子治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學稻田内科教室
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=5
article-no=
start-page=1459
end-page=1482
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1932
dt-pub=19320531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Histophathologie der japanischen epidemischen Encephalitis
kn-title=流行性腦炎ノ病理學的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Auf Grund der anatomischen Untersuchung von 8 Fällen der epidemischen Encephalitis, die Verf. im Laufe von 1924 bis 1929 beobachtet hat, kommt er zu folgenden Schlüssen. 1. Die Fälle lassen sich nach ihrem klinischen Verlaufe sowie ihrem histologischen Charakteristikum in drei Gruppen einteilen. Die erste verläuft stürmisch und kennzeichnet sich histologisch durch die Infiltration der Leukocyten und ihre Einstreuung ins Nervenparenchym. Die Gefässwandelemente und Ganglienzellen können dabei ganz unversehrt bleiben. Im weiteren Verlaufe, wo an den Ganglienzellen die degenerativen Erscheinungen zum Vorschein kommen, treten erst die Durchwandlung der histiocytären Phagocyten ins Parenchym und die Wucherung der Hortegaschen Glia auf. Die zweite Gruppe stellt den höchsten Gipfel des Krankheitsprozesses dar. Es entwickeln sich mannigfaltige Erscheinungen, wie die akuten Ganglienzellveränderungen verschiedener Stärke, die lymphocytären sowie plasmazellulären Infiltretionen, die meist knötchenbildenden Gliareaktionen usw. Die dritte Gruppe repräsentiert das chronische Stadium. Die Ganglienzellen weisen die schweren degenerativen Veränderungen auf oder fallen einfach aus, wobei die infiltrativen Vorgänge und Gliaherde in den Hintergrund treten. Keine besondere sekundäre Abräumerscheinung lässt sich merken. 2. Wenn auch der Krankheitsprozess die graue Substanz bevorzugt, so ist doch auch das Mark in Mitleidenschaft gezogen. Am stärksten sind der Thalamus (!!) und die Substantia nigra befallen; die anderen Hirngebiete, insbesondere die Gross- sowie Kleinhirnrinde, das Striatum, das Pallidum, der rote Kern, das Stammhirn u. a. beteiligen dem Krankheitsprozesse in wechselnder Stärke. 3. Bei typischen Fällen zeigt die sog. japanische Encephalitis den eklatanten Gegensatz zur Economoschen Encephalitis. Bei unseren Fällen treten die infiltrativen Erscheinungen meist in den Vordergrund, die bei der Economoschen Krankheit mehr nebensächliche Rolle spielen. Bei der Economoschen Encephalitis verteilen sich die Gliaherde im Gegensatz zu unseren immerhin diffus und haben geringere Neigung zur Knotenbildung. Was den Lieblingssitz des Krankheitsprozesses angeht, so müssen wir bei unseren Fällen zuerst den Thalamus nennen, während die Economosche Krankheit die Umgebung des Ventrikelsystems bevorzugt. Die Grosshirnrinde zeigt bei der Economoschen Encephalitis als Regel rein degenerative Veränderung. Bei unserer Form vermisst man dagegen nur ausnahmsweise deutliche Erscheinungen. Die Gliaherde in der Kleinhirnrinde, im Ponsfuss und in der unteren Olive gehören bei der Economoschen Encephalitis zur Seltenheit. Was zwischen den beiden gemeinsam ist, ist lediglich die schwere Veränderung in der Substantia nigra. 4. Nach alldem dürfen wir nicht ohne weiteres annehmen, dass die beiden Encephalitiden zwei ganz andere Krankheitsformen darstellen. Denn selbst bei uns, insbesondere bei atypischen kleinen Epidemien oder bei sporadischem Auftreten, treffen wir Fälle, bei denen die Beteiligung der Gross- sowie Kleinhirnrinde auffällig geringfügig, die Wand des dritten Ventrikels dagegen am stärksten befallen ist, zumal mit fast reiner hochgradiger Gliaproduktion. Andererseits können wir aus dem Schrifttum, wie das allbekannte Economos Werk auch zeigt, entnehmen, dass bei der europäischen Encephalitis, besonders am Anfang ihrer Epidemie, manchmal sicher akute Fälle zur Beobachtung kamen, die in der histopathologischen Nuance unserem Typ sehr nahe standen. Es besteht also noch eine, durchaus keine entfernteste Möglichkeit, dass die beiden Formen nach der Art sowie dem Alter der herrschenden Epidemien in der Natur und Lokalisation des Prozesses von den wohlbekannten, klassischen Bilden ziemlich weit abweichen können.
en-copyright=
kn-copyright=

en-aut-name=TakenoKazuo
en-aut-sei=Takeno
en-aut-mei=Kazuo
kn-aut-name=武野一雄
kn-aut-sei=武野
kn-aut-mei=一雄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學精神病學教室
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=1
article-no=
start-page=129
end-page=144
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1932
dt-pub=19320131
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Zur Frage der Differential-diagnose zwischen dem postencephalitischen Parkinsonismus und der Paralysis agitans
kn-title=「パルキンソニスムス」ト震顫麻痺トノ異同ニ就テ
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Die Arbeit gibt einen Überblick über die klinische und pathologische Histologie von 8 Fällen der Encephalitis chronica, 8 Fällen genuiner Paralysis agitans und 1 Fall seniler Muskelstarre als Teilerscheinung einer senilen Demenz. Die Arbeit hat zum Zweck noch einmal die histologischen und lokalisatorischen Unterscheide bei den genannten Krankheitsformen darzustellen und die gefundenen Veränderungen zu vergleichen mit der symptopathologischen Eigenart des klinischen Bildes. Ein Überblick über die Untersuchungsresultate zeigt uns, das die beiden Krankheitsformen Encephalitis chronica und genuine Paralysis agitans in der histopathologischen Prozessart und in der Lokalisation verschieden sind. Bei der Encephalitis chronica handelt es sich um einen langsam fortschreitenden degenerativen Prozess mit hochgradigem Ausfall der Ganglienzellen, stärkerer Gliareaktion bis zur Gliafasernarbenbildung. Dabei spielt die Verfettung des Parenchyms keine wesentliche Rolle. Leichte lymphozytäre Infiltrate können dabei in Erscheinung treten. Die Hauptlokalisation der Veränderungen ist die Substanzia nigra mit Ausstrahlungen in den Hypothalamus. Das Striopallidum kann ganz frei sein, kann sich aber auch in Ausnahmefällen stärker an dem Prozess beteiligen, ebenso die Olive und das Dentatum. Die Kleinhirnrinde ist relativ wenig geschädigt. Die Grosshirnrinde bietet gewöhnlich leichte architektonische Störungen ohne alle Charakteristica. Es bleibt dabei fraglich, ob diese Störungen in direktem Zusammenhang stehen mit dem Agens der Encephalitis oder indirekt ausgelöst sind durch Begleitumstände der Krankheit, besonders durch die Stoffwechselstörung. In allen Fällen bietet der Prozess keine ruhige Narbe, sondern noch progressive, aktive Veränderungen, die in ihrer Lebhaftigkeit stark wechseln können. Wir stehen auf dem von Jakob von jeher eingenommenem Standpunkte, dass diese Parenchymentartung der Ausdruck einer noch fortschreitenden Krankheit ist, die wahrscheinlich mit dem ursächlichen Agens in Zusammenhang steht. Bei der genuinen Paralysis agitans handelt es sich um einen schweren Verfettungsprozess des nervösen Parenchyms, wobei die gliösen Begleiterscheinungen gewöhnlich nicht sehr hochgradig entwickelt sind. Dieser Verfettungsprozess ist in erster Linie im Striatum und Pallidum lokalisiert und führt im Striatum regelmässig zu einer stärkeren Schädigung der grossen Ganglienzellen. Die Substanzia nigra kann völlig unverändert sein, kann aber auch mehr herdförmig-leichtere oder schwere Entartungen bieten; dabei steht aber gleichfalls der Verfettungsprozess im Vordergrunde und das histologische Gesamtbild ist ein ganz anderes wie das der Encephalitis chronica. Ganz gewöhnlich ist der Thalamus, namentlich der laterale Thalamuskern, stark mit geschädigt, manchmal auch die Olive, das Dentatum und die Kleinhirnrinde. Die Grosshirnrinde bietet gleichfalls Parenchymverfettung mit zum Teil deutlichen architektonischen Störungen, wobei Drusen und Alzheimer'sche Fibrillenveränderungen im Sinne der gewöhnlichen senilen Veränderungen fehlen. Nur in einem der oben erwähnten Fälle fanden sich diese Begleiterscheinungen einer gewöhnlichen senilen Demenz, sodass dieser Fall im Sinne Jakobs als senile Muskelstarre mit seniler Demenz aufzufassen ist. Der Parenchymprozess der gewöhnlichen Paralysis agitans hat mit dem senilen Involutionsvorgang die starke Parenchymverfettung gemein, es fehlen ihm aber für gewöhnlich die anderen regelmässigen Begleiterscheinungen der senilen Demenz. Ganz im allgemeinen zeigt sich kein deutlicher Parallelismus zwischen der Schwere der klinischen Erscheinungen und der Schwere des anatomischen Bildes. So sahen wir in einem Falle der Encephalitis chronica die Substanzia nigra noch stellenweise sehr gut erhalten und trotzdem war dieser Fall durch starken Parkinsonismus aus gezeichnet. Auch die Paralysis agitaus-Fälle bieten keinen regelmässigen Parallelismus zwischen Schwere des klinischen und anatomischen Bildes, besonders wenn man einseitig die Veränderungen im Striopallidum bewertet. Auch bestehen dabei starke Differenzen in Markscheiden, Fett-und Zellbilde.
en-copyright=
kn-copyright=

en-aut-name=TakenoKazuo
en-aut-sei=Takeno
en-aut-mei=Kazuo
kn-aut-name=武野一雄
kn-aut-sei=武野
kn-aut-mei=一雄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Hamburg大學Friedrichsberg精神病學教室病理部
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=4
article-no=
start-page=785
end-page=796
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1933
dt-pub=19330430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Über das Mesostriatum beim Huhn
kn-title=家鶏ノMesostriatumニ就テ
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bei Hühnern zerstörte der Verfasser das Mesostriatum verschiedentlich und liess die Tiere 3 Wochen lang weiter leben, um dann sie zu töten und ihre Gehirne mit Hilfe der Marchischen Methode zu untersuchen. Daraus ergibt sich das Folgende: 1) Das Mesostriatum verbindet sich mit dem Ektostriatum. 2) Es gibt Fasern, die sich vom Mesostriatum nach dem Brachium begeben und hier endigen. 3) Das Mesostriatum lässt keine Fasern entstehen, die oralwärts nach dem Hyper striatum und Epistriatum ziehen oder Caudalwärts den Nucleus rotundus erreichen. 4) Die beiderseitigen Brachii verbinden sich miteinander.
en-copyright=
kn-copyright=

en-aut-name=KondôTorao
en-aut-sei=Kondô
en-aut-mei=Torao
kn-aut-name=近藤寅夫
kn-aut-sei=近藤
kn-aut-mei=寅夫
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=12
article-no=
start-page=3286
end-page=3323
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1935
dt-pub=19351231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studien über die Morphogenese des Gehirns bei Kaninchenembryonen
kn-title=家兎胎兒腦ノ形態學的發生ニ關スル研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Verfasser hatte schon auf Grund seiner morphologischen Studien des Gehirns bei den Vögeln (Uroloncha domestica Flower und Hirundo rustica gutturalis) genaue Ergebnisse veröffentlicht. Da es aber vom Standpunkte der vergleichenden Entwicklungsgeschichte nötig ist, auch den Verlauf dieses Vorganges bei den Säugetieren festzustellen, so hat Verfasser über die Morphogenes des Gehirns bei Kaninchenembryonen Untersuchungen angestellt. Er erhielt folgende Resultate: 1) Der Neuroporus anterior verschliesst sich bei einem Embryo von 9 Tagen mit 13 Ursegmenten, der Neuroporus posterior bei einem Embryo von 9 1/2 Tagen mit 22 Ursegmenten, Der Neuropurus anterior schliesst sich also früher als der Neuroporus posterior; dies ist anders als bei den Vögln, bei denen sich der Neuroporus posterior früher verschliesst. 2) Der kraniale Teil des Nervenrohres bildet das Prosencephalon bei einem 8 Tage und 18 Stunden alten Embryo mit 9 Ursegmenten, das Mesencephalon bei einem 8 Tage und 20 Stunden alten mit 11 Ursegmenten, das Rhombencephalon bei einem 9 Tage alten mit 13 Ursegmenten; dadurch entstehen 3 primäre voneinander getrennte Hirnbläschen. Die 3 primären Hirnbläschen entstehen also nicht gleichzeitig; zuerst entsteht das Prosencephalon, dann das Mesencephalon, schliesslich das Rhombencephalon. Dieses Verhältnis ist bei den Säugern und bei den Vögeln ganz gleichartig. 3) Das Prosencephalon teilt sich ins Telencephalon und Diencephalon bei einem Embryo von 10 1/2. Tagen mit 32 Ursegmenten, das Rhombencephalon teilt sich ins Metencephalon und Myelencephalon am 12. Tage bei einem Embryo mit 46 Ursegmenten. Telen- und Diencephalon bilden sich also früher als Meten- und Myelencephalon, d. h. es ist ebenso wie bei den Vögeln. 4) Über die Grosshirnhemisphäre: Bei einem Embryo von 12 Tagen mit 46 Ursegmenten bildet sich ein longitudinaler Sulcus hemisphäricus in der dorsalen Wand des Telencephalon, durch welchen die dorsalen und lateralen Wände des Telencephalon in eine linke und rechte Hemisphäre geteilt werden. Der Hohlraum der Hemisphäre erweitert sich zum Seitenventrikel.
Bei einem Embryo von 14 Tagen bildet die ventrale Innenwand der Hemisphäre das Corpus striatum ventrale, ihre laterale Innenwand das Corpus striatum laterale. Das Corpus striatum ventrale nähert sich der Lamina terminalis und bildet mit ihr das Foramen Monroi. In diesem Stadium wird auch das Gebiet des Telencephalon medium deutlich, indem seine dorsale Wand von Lamina terminalis, seine ventralen und lateralen Wände vom Corpus striatum ventrale geformt werden. Der Hohlraum des Telencephalon medium stellt das orale Ende des 3. Ventrikels dar, welcher vermittelst des Foramen Monroi in Seitenventrikel geöffnet ist. Bei einem Embryo von 16 Tagen teilt die kraniale Ventralwand der Hemisphäre das Rhinencephalon ab. Da sich das Corpus striatum mit dem Thalamus opticus des Diencephalon verbindet, so ist die Wand des Foramen Monroi von Corpus striatum ventrate, Talamus opticus und Lamina terminalis gebildet. Die dorsale Wand der Hemispäre bildet das Pallium und ihre mediale Wand den Hippocampus. Aus der Lamina terminalis entsteht die Paraphyse. Das Velum transversum bildet mit dem Mesenchym den Plexus chorioideus des Seitenventrikels. 5) Über das Diencephalon: Bei einem Embryo von 10 1/2 Tagen mit 32 Ursegmenten beldet das kaudale Ende der ventralen Wand des Diencephalon das Tuberculum posterius, ihr kaudaler Teil das Tuber mammillare. Bei einem Embryo von 14 Tagen bildet ein Teil der dorsalen Wand des Diencephalon die Epiphyse, ihre grosse dorsale Wandpartie teilt sich in Parencephalon und Synencephalon. Der Hohlraum des Diencephalon nimmt bedeutend am sinistro-dexteren Durchmesser ab und bildet den 3. Ventrikel. Bei einem Embryo von 16 Tagen bildet der dorsale Teil der lateralen Wand des Diencephalon den Thalamus opticus, ihr ventraler Teil den Hypothalamus. Sulcus hypothalamicus od. Sulcus limitans, welcher vom Foramen Monroi und Recessus opticus ausgeht und miteinander zusammentrifft, läuft zwischen dem Thalamus opticus und Hypothalamus längsweise caudalwärts. 6) Über das Mesencephalon: Bei einem Embryo von 14 Tagen entwickelt sich ein sagittaler Sulcus medianus mesencephali in dem mittleren Teil der dorsalen Wand des Mesencephalon. Die ventrale Wand des Mesencephalon bildet den Pedunculus cerebri und lässt ein Paar Nervus oculomotorius anwachsen. Bei einem Embryo von 16 Tagen senkt sich der Sulcus medianus mesencephali noch tiefer. Von diesem Sulcus begrenzt, entstehen der linke und rechte Lobus opticus von der dorsalen und lateralen Wand des Mesencephalon. 7) Über das Metencephalon und Myelencephalon: Bei einem Embryo von 14 Tagen nehmen die Hohlräume des Metencephalon und des Myelencephalon am sinistrodexteren Durchmesser ab und stellen den 4. Ventrikel dar. Bei einem Embryo von 16 Tagen verdicken sich die dorsale und die laterale Wand des Metencephalon leistenartig und bilden das Cerebellum, seine ventrale Wand bildet die Pons; die dorsale Wand des Myelencephalon bildet mit dem Mesenchym den Plexus chorioideus des 4. Ventrikels, seine ventrale Wand mit der lateralen Wand die Medulla oblongata. 8) Von den Grenzen der sekundären Hirnbläschen bei den Vögeln sowie bei den Säugern. (A) Es entspricht die Telencephalon-Diencephalongrenze, die Eminentia telo-diencephalica, der Verbindungslinie zwischen dem Recessus opticus und dem Velum transversum. (B) Die Diencephalon-Mesencephalongrenze, die Eminentia mesodiencephalica, entspricht derjenigen Linie, welche quer vom Tuberculum posterius zur dorsalen Wand gezogen wird (C) Die Mesencephalon-Rhombencephalongrenze entsteht anfangs vom Sulcus rhombo-mesencephalicus, später vom Isthmus. (D) Die Metencephalon-Myelencephalougrenze zieht sich durch den Recessus lateralis. 9) Das Gehirn zeigt 3 Hirnbeugen bei den Vögeln wie auch bei den Säugern. Der Anteil der 3 Hirnbeugen und ihre entstandene Ordnung sind bei den Säugern und Vögeln gleich: anfangs nämlich erscheint die Kopfbeuge im Mesencephalon, dann die Nackenbeuge im kaudalen Ende des Rhombencephalon, endlich die Brückenbeuge in der kranioventralen Wand des Myelencephalon. 10) Was die Neuromerenzahl im Rhombencephalon betrifft, so findet Verfasser 6 Paar, sie ist also ganz ähnlich, wie sie Verfasser schon bei ben Vögeln beobachtet hat. Über die Verhältnisse zwischen den Neuromeren und Hirnuervenganglien im Rhombencephalon: (A) Ganglion semilunare des V. Hirnnerven wächst von II. Neuromerie aus. (B) Ganglion acustice-faciale des VII. und VIII. Hirnnerven von IV. Neuromerie. (C) Ganglion superias des IX. Hirnnerven von V. Neuromerie. (D) Ganglion jegulare des X. Hirnnerven wächst von der lateralen Wand des Rhombencephalon aus welche eaudalwärts als VI. Neuromerie liegt, ohne Beziehung zu der Neuromerie.
en-copyright=
kn-copyright=

en-aut-name=KochiTakeshi
en-aut-sei=Kochi
en-aut-mei=Takeshi
kn-aut-name=河内武
kn-aut-sei=河内
kn-aut-mei=武
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室胎生學研究室
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=8
article-no=
start-page=2159
end-page=2187
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1935
dt-pub=19350831
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studien über die Morphogenese der Hirnanlage (II. Mitteilung.) Über die Vögeln, besonders bei den Embryonen von Hirundo rustica gutturalis
kn-title=腦原基ノ形態學的發生ニ關スル研究（第2報）（鳥類特ニ燕Hirundo rustica gutturalisニ於ケル檢索）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Die Morphogenese der Hirnanlage habe ich schon früher bei Uroloncha domestica Flower untersucht und meine Meinung über, dieselbe unter Angabe der Resultate meiner Untersuchungen veröffentlicht. Da ich aber vom Gesichtspunkt der vergleichenden Entwicklungsgeschichte die Notwendigkeit der Studien auch bei anderen Vögeln erkannte, so untersuchte ich nun die Entwicklungsgeschichte der Hirnanlage bei Hirundo rustica gutturalis. Die Resultate der vorliegenden Untersuchungen lassen sich folgendermassen zusammenfassen: 1) Bei einem Embryo von 3.2mm grösster Länge mit 11 Urwirbelpaaren ist die Nervenrinne der Kaudalseite zum Nervenrohr verändert. Bei einem Embryo von 4.0mm grösster Länge mit 16 Urwirbelpaaren ist Neuroporus anterior der Kranialseite vollständig geschlossen. 2) Bei einem Embryo von 3.2mm grösster Länge mit 11 Urwirbelpaaren fand ich die Entstehung des Prosencephalon und Mesencephalon. Bei einem Embryo von 4.0mm grösster Länge mit 14 Urwirbelpaaren fand ich die Entstehung des Rhombencephalon; hier kann man die Entwicklung der 3 primären Hirnbläschen erkennen. 3) Bei einem Embryo von 5.3mm grösster Länge mit 24-25 Urwirbelpaaren fand ich das Prosencephalon in Telencephalon und Diencephalon zerlegt, bei einem Embryo von 4.0mm Nacken-Steisslänge mit 34-35 Urwirbelpaaren das Rhombencephalon in Metencephalon und Myelencephalon zerlegt; hier kann man an 5 sekundäre Hirnbläschen unterscheiden. 4) Bei einem Embryo von 4.0mm Nacken-Steisslänge mit 34-35 Urwirbelpaaren bildet das Telencephalon die Grosshirnhemisphäre; bei einem Embryo von 6.0mm Nacken-Steisslänge entwickelt sich das Rhinencephalon an der Vorderkante der Grosshirnhemisphäre. Die Innenfläche den Grosshirnhemishäre bildet das Corpus striatum, welches mit Lamina terminalis zusammen das Foramen Monroi bildet. 5) Bei einem Embryo von 4.0mm Nacken-Steisslänge mit 34-35 Urwirbelpaaren fand ich die Zerlegung des Diencephalon in Parencephalon und Synencephalon und die Entstehung der Epiphyse an der Dorsalwand des Parencephalon; bei einem Embryo von 9.5mm Nacken-Steisslänge bemerkte ich die Entstehung des Thalamus opticus an der Lateralwand und des Chiasma opticum an der Vorderwand des Diencephalon. 6) Bei einem Embryo von 6.0mm Nacken-Steisslänge bildet sie sich in beiderseitigen Lobus opticus um, da Sulcus medianus mesencephali sich an dem Medianteil der Dorsalwand des Mesencephalon entwickelt. Bei einem Embryo von 9.5mm Nacken-Steisslänge verdickt sich. die Vorderwand des Mesencephalon, um Crura cerebri zu bilden. 7) Bei einem Embryo von 9.5mm Nacken-Steisslänge fand ich, dass das Metencephalon sich an der Dorsal- und Lateralwand verdickt und die Kleinhirnplatte bildet, und dass die Vorderwand die Ponsanlage bildet. 8) a) Die Telencephalon- Diencephalongrenze wird innen durch Eminentia telodiencephalica gebildet, ihr entspricht die Vereinigungslinie des Recessus opticus und des Velum transversum. b) Die Diencephalon- Mesencephalongrenze ist innen durch Eminentia mesodiencephalica gebildet, die letztere läuft quer vom Tuberculum posterius bis in die Linie der Dorsalwand. c) Die Mesencephalon- Rhombencephalongrenze wird anfangs durch Sulcus rhombomesencephalicus und später durch den Isthmus gebildet. 9) Die Kopfbeuge entwickelt sich am frühesten im Mesencephalon eines Embryo von 4.0mm grösster Länge mit 16 Urwirbelpaaren. Bei einem Embryo von 4.0mm Nacken-Steisslänge mit 34-35 Urwirbelpaaren ist die Nackenbeuge an der Caudalseite des Rhombencephalon zu bemerken. Die Brückenbeuge entwickelt sich am spätesten bei einem Embryo von 6.0mm Nacken-Steisslänge von dem Myelencephalon. 10) Neuromerenzahl: Ich fand von diesen 4 Paare bei einem Embryo von 5.3mm grösster Länge mit 24-25 Urwirbelpaaren, 5 Paare bei einem Embryo von 4.5mm grösster Länge mit 30 Urwirbelpaaren, 6 Parren bei einem Embryo von 4.0mm Nacken-Steisslänge mit 34-35 Urwirbelpaaren. 11) Aus dem II Neuromerie entstammt das Ganglion. Semilunare der V Hirnnerven, und aus dem IV Neuromerie entspriugt das Ganglion acustico-faciale der VII u. VIII Hirnnerven.
en-copyright=
kn-copyright=

en-aut-name=KochiTakeshi
en-aut-sei=Kochi
en-aut-mei=Takeshi
kn-aut-name=河内武
kn-aut-sei=河内
kn-aut-mei=武
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室胎生學研究室
END

start-ver=1.4
cd-journal=joma
no-vol=50
cd-vols=
no-issue=3
article-no=
start-page=745
end-page=754
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1938
dt-pub=19380331
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Uber das sog. striäre Blutsyndrom
kn-title=所謂線状體血液症候ニ就テ
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Im Jahre 1923 beobachteteu Sato und Yoshimatsu ein eigenartiges Blutbild bei zwei Fällen von akuter Encephalitis epidemica, d.h. während die Oxydasereaktiou nach Winkler und Schultze positiv siud, war die Peroxydasereaktion nach Sato uud Sekiya (Kupfervitriollosung, danu Benzidin und H(2)O(2)) in den rnyeloischeu Leukozyten des strömenden Blutes negativ. In weiteren Versuchen mit Schädigung des Striatum von Kaninchen konnten sie das gleiche Blutbild hervorrufeu (sog. Peroxydasestich). Deshalb kam Sato nun auf die Vermutung, dass es sich bei diesem Blutsyndrom um Funktionestöungeu des Striatum irn Hirustamm handelu könnte, und nannte dieses Phänomen "striäres Blutsyndrom". Sie stellten dieses Blutsyndrom nur auf der Höhe des Krankheitsstadiums fest; bei Besserung des Krankheitsprozesses verschwand es wieder. Aus diesem Grunde machte Sato eiuen Vorschlag, dieses striäre Blutsyndrom auf die kliuische Herddiagnose des Hirns und die Prognosenbestimmung des Krankheitsprozesses anzuwenden. Hierauf untersuchten wir 83 Patienten mit akuter Encephalitis epidemica in verschiedenen Krankheitsstadieu, 16 P. mit Extrapyramidalsystemerkraukungen, 56 P. mit andereu akuten uud chroniechen Erkrankungen und Tiere nach Zerstörung des Striatum auf des sog. striäre Blutsyndrom, fanden es aber niemals.
Aus diesen Uutersuchungen kameu wir zun folgenden Schluss : Das sog. striäre Blutsyudrom uach Sato und Yoshimatsu ist für klinische Lokalisationsdiagnose des Hirns und Prognosenbestimmungen des Kraukheitsprozesses ungeeignet.
en-copyright=
kn-copyright=

en-aut-name=NakataFujio
en-aut-sei=Nakata
en-aut-mei=Fujio
kn-aut-name=中田富士男
kn-aut-sei=中田
kn-aut-mei=富士男
aut-affil-num=1
ORCID=

en-aut-name=FujiiToshio
en-aut-sei=Fujii
en-aut-mei=Toshio
kn-aut-name=藤井敏夫
kn-aut-sei=藤井
kn-aut-mei=敏夫
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學柿沼，北山内科教室

affil-num=2
en-affil=
kn-affil=岡山醫科大學柿沼，北山内科教室
END

start-ver=1.4
cd-journal=joma
no-vol=53
cd-vols=
no-issue=7
article-no=
start-page=1399
end-page=1421
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1941
dt-pub=19410731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studien über die Morphogenese der Hirnanlage (I. Mitteilung) Über die Vogeln, besonders bei den Embryonen von Anas domestica
kn-title=腦原基ノ形態學的發生ニ關スル研究（第1報）（鳥類特ニ家鴨Anas domesticaニ於ケル檢索）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mit der Morphogenese des Gehirnes der höheren Wirbeltiere haben sich schon viele, wie Malphigi, Haller, Beraneck, Rabl, Platt, Kupffer, G. Henrich, Kôchi, u.a. befasst, ihre Meinungen gehen aber in vielen Punkten auseinander, so das es gegenwartig noch kaum möglich ist, etwas Zuverlässiges darüber ausfindig zu machen. Darum habe ich über die Entwicklung des Gehirnes bei Embryonen von Anas domestica sorgfältige Untersuchung gestellt. Das Material wurde in Zenkerscher FluBigkeit fixiert und mit Boraxkarmin gefärft. Alles wurde in Paraffin ein-gebettet und in quere Serien von 10μ Dicke geschnitten. Die Plattenrekonstruktionsmodelle wurden nach der Born-Peter'schen methode angefertig. Die Resultate der vorliegenden Untersuchungen lassen sich folgendermassen zusammenfassen. 1) Der Neuroporus anterior verschlieBt sich bei einem Embryo von 4, 6mm grösster Länge mit 15 Ursegmenten, viergegen verschliesst sich der Neuroporus posterior bei einem Embryo von 6,0mm grosster Länge mit 21 Ursegmenten. 2) Bei einem Embryo von 3, 9mm grösster Länge mit 10 Ursegmenten fand ich die Entstehung des Prosencephalon und Mesencephalen. Bei einem Embryo von 4, 4mm grösster Länge mit 12 Ursegmenton fand ich die Entstehung des Rhombencephalon; hier kann man Entstehung der 3 primäre Hirnbläschen erkennen. 3) Bei einem Embryo von 7, 0mm grösster Länge mit 25-26 Ursegmenten trennt sich Prosencephalon in Telencephalon und Diencephalon, bei einem Embryo von 7,0 Nackensteisslänge mit 38-39 Ursegmenten das Rhombencephalon trennt sich in Metencephalon und Myelencephalon; hier kann man an 5 Sekundäre Hirn blaschen unterscheiden. 4) Bei einem Embryo von 7, 0mm Nacken-Steiss länge mit 38-39 Ursegmenten bildt das Telencephalon die GroBhirn-hemisphäre; bei einem Embryo von Scheitel-Steisslange 16, 0mm die Innenfläche den Grosshirnhemisphäre bildet das Corpus striatum, welches mit Lamina terminalis zusammen das Foramen Monroi bildet. 5) Bei einem Embryo von 7, 0 Nacken-steisslänge mit 38-39 Ursegmenten fand ich die Abtrennung des Diencephalon in Parencephalon und Synencephalon und Entstehung der Epiphyse an der Dorsalwand des Parencephalon; bei einem Embryo von 16,0mm Scheitel-Steisslänge bemerkt ich die Entstehung des Thalamus opticus an der Lateralwand und des Chiasma Opticum an der Vor-derwand des Diencephalon. 6) Bei einem Embryo von Scheitel-Steisslänge 8,0mm bildet das Mesencephalon sich in beiderseitigen Lobus opticus um, da Sulcus medianus mesencephali sich an dem Medianteil der Dorsalwand des Mesencephalon entwickelt. Bei einem Embryo von 16, 0mm Scheitel-Steisslänge verdickt sich die Ventralwand des Mesencephalon und bildet sich Penduculus cerebri. 7) Bei einem Embryo von 16, 0mm Scheitel-SteiBlänge fand ich, daB das Metencephalon sich an der Dorsal-und Lateral-wand verdickt und die Kleinhirnplatte bildet. und daB die Ventralwand die Ponsanlage bildet. 8) a) Die Telencephalon-Diencephalongrenze wird innen durch Eminentia telo-diencephalica gebildet, ihr entspricht die Vereinigungslinie des Recessus opticus und des Velum transversum. b) Die Diencephalon-Mesencephalongrenze ist innen durch Eminentia meso-diencephalica gebildet, die letztere lauft quer vom Tubercum posterius bis in die Linie der Dorsalwand. c) Die Mesencephalon-Rhombencephalon grenze wird anfangs durch Sulcus rhombo-mensencephalicus und sparter durch den Isthmus gebildet. 9) Die Kopfbeuge entwickelt sich am fruhesten im Mesencephalon eines Embryo von 4,6mm grösster Länge mit 15 Ursegmenten. Bei einem Embryo von 6,5mm Nacken-Steisslange mit 32-33 Ursegmenten ist die Nackenbeuge an der Caudalseite des Rhombencephalon zu bemerken. Die Brückenbeuge entwickelt sich spärteresten bei einem Embryo von 8,0mm Scheitel-Steisslänge von dem Myelencephalon. 10) Neuromerenzahl: Ich fand von diesen 5 Paare bei einem Embryo von 7,5mm grösster Länge mit 29-30 Ursegmenten, 6 Paare bei einem Embryo von 8,5 grösster Länge mit 36-37 Ursegmenten.
en-copyright=
kn-copyright=

en-aut-name=TasakaShigemi
en-aut-sei=Tasaka
en-aut-mei=Shigemi
kn-aut-name=田坂重實
kn-aut-sei=田坂
kn-aut-mei=重實
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室胎生學研究室
END

start-ver=1.4
cd-journal=joma
no-vol=54
cd-vols=
no-issue=2
article-no=
start-page=279
end-page=304
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1942
dt-pub=19420228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Stndien über die Morphogenese der Reptiline, besonderes bei den Embroyonene von Kreuzotter
kn-title=腦原基ノ形態學的發生ニ關スル研究（第3報）（爬蟲類特ニ蝮蛇Kreuzotterニ於ケル檢索）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Seit Edinger sind über die Entwieklung des Gehirns der Reptilien verhältnismässig wenige Arbeiten veröffentlicht. Wegen der Verschiedenheit des gegenstandes der Forschung sind auch die Ansichten sehr verschieden, Der Verfasser hat unter Leitung von Prof. Dr. J. Shikinami Untersuchungen über die morpbologische Entwicklung des Gehirns bei Embryonen von Kreuzotter angestellt und dabei folgende Resultate erzielt: 1) Bei einem Embryo von 2,5mm grösster Länge fand ich die Entetehung des Prosencephalop und Rhombencephalon; hier kann man die Entwieklung der 3 primären Hirnbläschen erkennen. 2) Das Prosencephalon teilt sich ins Telencephaion und Diencephalon bei einem Embryo von 3,5mm grösster Länge, das Rhombencephalon teilt sich ins Meten cephalon und Myelencephalon bei einem Embryo von 9, 0mm grösster Lange; hier kann man an 5 sekundäre Hirnblaschen unterscheiden. 3) Bei einem Embryo von 5,5mm grösster Länge bildet das Telencephalon die Grosshirnhemisphäie; bei einem Embryo von 10,0mm grösster Länge entwickelt sich das Rhinencephalon an der Vorderkante der Grosshirnhemisphare. Die Innenflache der Grosshirn hemisphäre bildet das Corpus striatum, welches mit Lamina terminalis zusammen das Foramen Monroi bildet. 4) Bei einem Embryo von 5, 5mm grösster Länge fand ich die Zerlegung des Diencephalon in Parencephalon und Synencephalon und die Entstehung der Epiphyse an der Dorsalwand des Parencephalon; bei einem Embryo von 10, 0mm grosster Lange bemerkt ich die Entstehung des Thalamus opticus an der Lateralwand und des Hypothalamus an der ventralwand des Diencephalon. 5) Bei einem Embryo von 10,0mm grösster Länge bildet sie sich in beiderseitigen Lobus opticus um, da Sulcus medianus mesenoephali sich an dem Medianteil der Dorsalwand des Mesencephalon entwickelt. Bei einem Embryo von 20,0mm grosster Lange verdickt sich die Ventralwand des Mesencephalon, um Pendunculus cerebri zu bilden. 6) Bei einem Embryo von 10, 0mm grösster Länge fand ich, dass das Metencepholon sich an der Dorsal- und Lateral- wand verdickt und die Kleinhirnplatte bildet, und dass die Ventralwand die Ponsanlage bildet. 7) a) Die Telencephalon- Diencephalongrenze wird innen durch Eminentia telodiencephalica gebildet, ihr entspricht die Vereinigungslinie des Recessus opticus und des Velum transversum. b) Die Diencephalon- Mesencephalongrenze ist innen durch Eminentia mesodiencephalica gebildet, die letztere läuft quer von Tuberculum posterius bis in die Linie der Dorsalwand. c) Die Mesencephalon-Rhombencephalongrenze wird aufangs durch Sulcus rhombomesencephalicus und später durch den Isthmus gebildet. 8) Die Kopfbeuge entwickelt sich am frühesten im Mesencephalon eines Embryo von 2,5mm gröosster Länge. Bei einem Embryo von 5,5mm grösster Länge ist die Nackenbeuge an der Caudalseite des Rhombencephalon zu bemerken. Die Brückenbeuge entwickelt sich am spätesten bei einem Embryo von 9,0mm grösster Lange von dem Myelencephalon. 9) Was die Neuromehrenzahl im Rhombencephalon betrifft so findet Verfasser 6 Paar, sie ist also ähnlich, wie sie Verfasser schon bei den Vögeln beobachtet hat. 10) Ganglion semilunare des V. Hirnnerven wächst von II. Neuromeric aus. Ganglion acusticofaciale des VII. und VIII. Hirnnerven von IV. Neuromerie.
en-copyright=
kn-copyright=

en-aut-name=TasakaShigemi
en-aut-sei=Tasaka
en-aut-mei=Shigemi
kn-aut-name=田坂重實
kn-aut-sei=田坂
kn-aut-mei=重實
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室胎生學研究室
END

start-ver=1.4
cd-journal=joma
no-vol=54
cd-vols=
no-issue=2
article-no=
start-page=259
end-page=278
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1942
dt-pub=19420228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studien über die Morphogenese der Hirnanlage (II. Mitteilung) Über die Vögeln, besonders bei den Embryonen von Taeniopygia castonitus
kn-title=腦原基ノ形態學的發生ニ關スル研究（第2報）（鳥類殊ニ錦花鳥Taeniopygia castonitusニ於ケル檢索）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Der Verfasser hat unter Leitung von Prof. Dr. J. Shikinami Untersuchungen über die morphorogische Entwicklung des Gihirns bei Embryonen von Taeniopygia castonitus angestellt und dabei folgende Resultate erzielt. 1) Bei einem Embryo mit 13 Urwirbelpaaren ist die Nervenrinne der Kaudalseite zum Nervenrohr verändert. Bei einem Embryo mit 15 Urwirbelpaaren ist Neuroporus anterior der Kranialseite vollständig geschlossen. 2) Das Vorderhirnbläschen tritt sich auf am frühesten bei einem Embryo mit 9 Wirbelpaaren; dann erscheint das Mittelhirnbläschen bei einem Embryo mit 10 Urwirbelpaaren und endlich entsteht das Rautenhirnbläschen bei einem Embryo mit 13 Urwirbelpaaren. So entwickeln sich die 3 Primäre Hirnbläschen. 3) Bei einem Embryo mit 23 Urwirbelpaaren fand ich das Prosencephalon in Telencephalon und Diencephalon zerlegt, bei einem Embryo mit 35-36 Urwirbelpaaren das Rhombencephalon in Metencephalon und Myelencephalon zerlegt; hier kann man an 5 sekundäre Hirnbläschen unterscheiden. 4) Bei einem Embryo mit 35-36 Urwirbelpaaren bildet das Telencephalon die Grosshirnhemisphäre; bei einem Embryo von 5.3mm Nacken-Steisslänge entwickelt sich das Rhinencephalon an der Vorderkante der Grosshirnhemisphäre. Die Innenfläche der Grosshirnhemisphäre bildet dar Corpus striatum, welches mit Lamina tarminalis zusammen das Foramen Monroi bildet. 5) Bei einem Embryo mit 35-36 Urwirbelpaaren fand ich die Zerlegung des Diencephalon in Parencephalon und Synencephalon und die Entstehung der Epiphyse an der Dorsalwand des Parencephalon; bei einem Embryo von 9.0mm Nacken-Steiss länge bemerkt ich die Entstehung des Thalamus opticus an der Lateralwand und des Chiasma opticum an des Vorderwand des Diencephalon. 6) Bei einem Embryo von 5.0mm Nacken-Steisslänge bildet sie sich in beiderseitigen Lobus opticus um, da Sulcus medianus mesencephali sich an dem Medianteil der Dorsalwand des Mesencephalon entwickelt. Bei einem Embryo von 9.0mm. Nacken-Steisslänge verdickt sich die Vorderwand des Mesencephalon, um Crura cerebri zu bilden. 7) Bei einem Embryo von 9.0mm. Nacken-Steisslänge fand ich, dass das Metencephalon sich an der Dorsal-und Lateral-wand verdickt und die Kleinhirnplatte bildet, und dass die Vorderwand die Ponsanlage bildet. 8) a) Die Telencephalon-Diencephalongrenze wird innen durch Eminentia telodiencephalica gebildet, ihr entspricht die Vereinigungslinie des Recessus opticus und des Velum transversum. b) Die Diencephalon-Mesencephalongrenze ist innen durch Eminentia mesodienaphalica gebildet, die letztere lauft quer vom Tuberculum posterius bis in die Linie der Dorsalwand. c) Die Mesencephalon-Rhombencephalongrenze wird Anfangs durch Sulcus rhombomesencephalicus und später durch den Isthmus gebildet. 9) Die Kopfbeuge entwickelt sich am frühesten im Mesencephalon eines Embryo mit 15 Urwirbelpaaren. Bei einem Embryo mit 23 Urwirbelpaaren ist die Nackenbeuge an der Caudalseite des Rhombencephalon zu bemerken. Die Bruckenbeuge entwickelt sich am spateresten bei einem Embryo von 5.0mm. Nacken-steisslange von dem Myelencephalon. 10) Neuromerenzahl; Ich fand von diesen 4 Paare bei einem Embryo mit 23 Urwirbelpaaren, 5 Paare bei einem Embryo mit 24-25 Urwirbelpaaren, 6 Paare bei einem Embryo mit 35-36 Urwirbelpaaren.
en-copyright=
kn-copyright=

en-aut-name=TasakaShigemi
en-aut-sei=Tasaka
en-aut-mei=Shigemi
kn-aut-name=田坂重實
kn-aut-sei=田坂
kn-aut-mei=重實
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山醫科大學解剖學教室胎生學研究室
END

start-ver=1.4
cd-journal=joma
no-vol=66
cd-vols=
no-issue=6
article-no=
start-page=1091
end-page=1106
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1954
dt-pub=19540630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on Hereditary Nervous Diseases Part I. On Huntington's Chorea
kn-title=遺伝神経病の研究 第1篇 Huntington舞踏病に就て
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=From my investigations of five families subject to Huntington's Chorea, I have come to the following conclusions. 1. Two of them are considered as double phenotypes of chorea and schizophrenia. Others remind us of double phenotypes of ptosis and the so-called lethal factors. 2. Four families are found to be subject to dementia and psychopathia as much as to choreatic movement; one family is liable only to psychopathia. Two families have a tendency to attempt suicide, commit murder and other crimes. 3. A case of anatomical examination shows a remarkable change in the cerebellar cortex, dentatum and nucleus olivalis, in spite of the slight change in striatum and cerebral cortex. Cases of change in nucleus olivaris may perhaps be rare. 4. Such "Disease Gene" as chorea Huntingtoni or "Lethal Factor", I suppose, is caused by the degradation or loss of functions of "Normal Gene" through mutation. Can it not be reasoned, then, that the very existence of "Disease Gene" brings the functions of "Normal Gene" into relief?
en-copyright=
kn-copyright=

en-aut-name=OchoYakichi
en-aut-sei=Ocho
en-aut-mei=Yakichi
kn-aut-name=大重彌吉
kn-aut-sei=大重
kn-aut-mei=彌吉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部精神病学教室
END

start-ver=1.4
cd-journal=joma
no-vol=71
cd-vols=
no-issue=8-1
article-no=
start-page=4761
end-page=4768
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1959
dt-pub=19590810
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A Study on the Mechanism of Chlorpromazine Action on the Brain
kn-title=脳髄に於けるクロールプロマジン作用機序についての研究 第3編 C. P. 長期少量投与時に於ける犬脳の病理組織学的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ever since 1952 when Delay, Deniker and Heal first used chlorpromazine for various psychiatric patients, its clinical effect has come to be recognized. And as is wellknown it is now one of important drugs in the treatment of patients with mental illness. Believing that the clarification of the mechanism acting on the brain will still further the pathological study in endogenous psychoses, the author performed a series of experiments with dog, in which he studied clinical symptoms and side-effecects at the time of chlorpromazine administration and also carefully analyzed the results of histopathological findings on the brain for the purpose of elucidation of the mechanism of chlorpromazine acting on the brain. Namely, dogs were divided into two groups: the A-group given a large dose of chlorpromazine for a short period of time; and the B-group given a small does of chlorpromazine for a long time. 1. For the A-group, grown-up dogs and young dogs were selected to the total of nine dogs, and in order to give shockwise 43-133 mg/kg chlorpromazine was injected into the artery, vein or muscle. As the result the clinical stage can be divided into five stages: 1. somnolent stage; 2. lethargic stage; 3. paralytic stage; 4. dyspnea stage; and 5. agonal stage. All of them died within several days. It was revealed that various symptoms of motor disturbances were most apt to appear in the lethargid stage. Especially the young dog No.8 showed a marked torsion dystonia-like symptoms at this atage and these symptoms persisted thereafter. All of them were sacrificed by decapitation six hours after the injection, and removing and fixing the brains, histological specimens were prepared. 2. For the B-group two adult dogs were selected and 10 mg/kg chlorpromazine was injected every day intramuscularly. Although clinical symptoms could not be divided into different stages, there was a period when they became somnolent. There were decapitated 31 days after the start of experiment and tissue specimens were prepared in the same way as mentioned above. By comparing there clinical symptoms in dogs with those observed in hyman cases, the author studied the mechanism of chlorpromazine action in the brain. In the histopathologisal investigations specimens were stained with hematoxylin-eosin, azo-carmine, Nissl stain, myelin sheath stain, and fat stain (Sudan III). In the A-group changes changes appearing diffusely in the entire brain, the so-called acute changes, and those of nerve cells caused bue to the changes in blood vessels were recognized. Sites especially marked for such changes were in the corpus striatum, thalamus, putamen, globus pallidum, nucleus niger, nucleus ruber, corpus mammillaris, nucleus amygdae and a portion of cerebral cortex. In comparison of these changes with pathoanatomy of torsion dystonia in the literatures, the changes mentioned above seemed to substantiate torsion dxstonia-like symptoms. In the B-group their characteristic changes were chronic atrophy of nerve cells and demyelinating plaques in cortical medullary radiation. Moreover, these changes were found to appear selectively at a definite portion of the brain; and it is believed that these findings offer the clue for the acting mechanism of chlorpromazine in the hrain. Finally for the purpose of explaining summarily the acting mechanism of chlorpoomazine the author discussed first the sites of chlorpromazine action, its distribution in the brain, and then the acting mechanism of chlorpromazine reported in available literatures, and also made a comparison between the results obtained by other investigators and those in the present experiment as well as the correlation with clinical symptoms.
en-copyright=
kn-copyright=

en-aut-name=ShimizuHidenori
en-aut-sei=Shimizu
en-aut-mei=Hidenori
kn-aut-name=清水英詮
kn-aut-sei=清水
kn-aut-mei=英詮
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=11-12
article-no=
start-page=977
end-page=989
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198912
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies of guanidinoethanesulfonic acid induced convulsions - Effect of guanidinoethanesulfonic acid on monoamines in the mouse brain -
kn-title=Guanidinoethanesulfonic acid誘発痙攣に関する研究―特に脳内モノアミンにおよぼす影響―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Guanidinoethanesulfonic acid (GES) is known to induce convulsive seizures when administered intracisternally into rabbits and cats. I examined the effects of GES on behavior, electroencephalogram and brain monoamine levels after intraventricular injection into mice. When GES was intraventricularly injected into mice, focal clonic movements of the face, vibrissae and ears, as well as twitchings of limbs were observed 0.5-1 min after injection. Hypersensitivity was observed until 7 min after the injection, after which the mice behaved in a normal way. It is also observed that GES induced sporadic spike discharges in the electroencephalogram. The latency and duration of the appearence of spike discharges showed considerable individual variation. The latency was from 0 to 5 min, and the duration was from 5 to 90 min. No spike discharge was observed in the saline injected animals. The 5-hydroxytryptamine (5-HT) level decreased in the hippocampus, diencephalon, pons-medulla oblongata and cerebellum 5 min after injection, and recovered to the control level 10 min after the injection. No change in the norepinephrine (NE) and dopamine (DA) levels was found after GES injection. 5-hydroxyindoleacetic acid increased in the striatum and cerebellum 5 min after injection. It is thought that the GES injection enhances the release of 5-HT in the striatum and cerebellum, although the mechanism of the decrease of 5-HT in the hippocampus, diencephalon and pons-medulla oblongata is unclear. These results indicate that the GES induced convulsive seizure is related to 5-HT neurons, not NE or DA neurons.
en-copyright=
kn-copyright=

en-aut-name=WatanabeShunji
en-aut-sei=Watanabe
en-aut-mei=Shunji
kn-aut-name=渡辺駿二
kn-aut-sei=渡辺
kn-aut-mei=駿二
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門教室
en-keyword=guanidinoethanesulfonic acid
kn-keyword=guanidinoethanesulfonic acid
en-keyword=convulsion
kn-keyword=convulsion
en-keyword=brain monoamines
kn-keyword=brain monoamines
en-keyword=5-hydroxytryptamine
kn-keyword=5-hydroxytryptamine
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=11-12
article-no=
start-page=1373
end-page=1384
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199012
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effect of N-methyl-D-aspartic acid on amino acids levels in the mouse brain
kn-title=N-メチル-D-アスパラギン酸脳室内投与のマウス脳内アミノ酸への影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The naturally-occurring dicarboxylic amino acids, L-glutamate (Glu) and L-aspartate, are the principal neurotransmitter candidates for excitatory synaptic transmission in vertebrate central nervous systems. The receptors activated by these amino acids are classified by their most selective and potent agonists, i.e., N-methyl-D-aspartic acid (NMDA), kainic acid, and quisqualic acid. In this study, I examined the effects of NMDA on behavior, electroencephalogram (EEG), and brain amino acids levels after intraventricular injection in mice. When NMDA was intraventricularly injected into mice, running fits were observed 10-30 seconds after injection, followed by a sedative phase and returned to a normal behavior within 15-20 minutes after injection. In the EEG, middle voltage fast waves were observed 10-20 seconds after injection, followed by EEG suppression for a few minutes and the appearance of high voltage slow waves 4-5 minutes after injection. About 20 minutes after the injection the EEG was normal. No spike discharge was observed during this observation. Glu levels increased in the hippocampus during running fits, while GABA levels decreased in the cerebellum and hippocampus before running fits, and increased in the cerebellum 10 minutes after NMDA injection. The taurine level decreased in the striatum before running fits. All amino acids observed recovered to control levels 60 minutes after NMDA injection. These results indicate that the NMDA-induced running fits are not accompanied by spike discharges in the EEG, and are related to Glu and GABA neurons.
en-copyright=
kn-copyright=

en-aut-name=OkamuraYuji
en-aut-sei=Okamura
en-aut-mei=Yuji
kn-aut-name=岡村裕司
kn-aut-sei=岡村
kn-aut-mei=裕司
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=N-methyl-D-aspartic acid
kn-keyword=N-methyl-D-aspartic acid
en-keyword=excitatory amino acids
kn-keyword=excitatory amino acids
en-keyword=inhibitory amino acids
kn-keyword=inhibitory amino acids
en-keyword=running fits
kn-keyword=running fits
en-keyword=mouse EEG
kn-keyword=mouse EEG
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=7-8
article-no=
start-page=997
end-page=1005
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199008
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Toxicity of organic phosphates and chloronaphthalenes Part 2. Effect of chlorpyrifos on cholinesterase activity in rats
kn-title=白アリ防除剤に関する実験的研究 第2編 クロルピリホスのラットにおけるコリンエステラーゼ活性におよぼす影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inhibition of cholinesterase (ChE) activity was examined by experiments on enzyme activity of ChE of rat administered intraperitoneally chlorpyrifos and enzyme kinetic study of ChE in plasma. Plasma ChE activity was inhibited more highly than erythrocyte ChE activity in rat 12 hrs after administration. Plasma ChE activity was recovered 1 month after administration but erythrocyte ChE activity was not recovered. No difference between frontal cortex and striatum ChE activity was recognized. Changes in brain ChE activity was similar to those in erythrocyte ChE activity. PAM affected the inhibition of ChE activity by chlorpyrifos on 3 hrs after administration but other ChE activities were not.
Uncompetitive inhibition between chlorpyrifos and ChE was proved by Lineweaver-Burk plots.
Inhibition of ChE isoenzyme was found on bands 4 and 7 by electrophoresis. These results suggest that plasma ChE was effective for exposure monitoring and erythrocyte ChE was effective for effect monitoring.
en-copyright=
kn-copyright=

en-aut-name=SakaiRitsue
en-aut-sei=Sakai
en-aut-mei=Ritsue
kn-aut-name=酒井律江
kn-aut-sei=酒井
kn-aut-mei=律江
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部公衆衛生学教室
en-keyword=クロルピリホス
kn-keyword=クロルピリホス
en-keyword=コリンエステラーゼ活性
kn-keyword=コリンエステラーゼ活性
en-keyword=血球・血漿・脳
kn-keyword=血球・血漿・脳
en-keyword=PAM
kn-keyword=PAM
en-keyword=アイソザイム
kn-keyword=アイソザイム
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=5-6
article-no=
start-page=583
end-page=592
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199006
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The effects of selective D-1 and D-2 dopamine antagonists on methamphetamine-induced changes in substance P and TRH receptor binding
kn-title=Methamphetamine投与による脳内substance P系, TRH系の変化におよぼす選択的D-1, D-2遮断薬の効果
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effects of pretreatment with either SCH 23390, a selective D-1 antagonist or YM-09151-2, a selective D-2 antagonist, on methamphetamine (MAP)-induced changes in the substance P and TRH system were investigated. A single dose of 4 mg/kg of MAP reduced the striatal level of substance P 30 min after injection. This reduction was reversed by pretreatment with YM-09151-2 but not with SCH 23390. Repeated administration of 4 mg/kg of MAP for 14 days reduced specific substance P and TRH binding in the striatum at 1 h, but not at 48 h, after the last injection. The reduction of striatal substance P receptor binding was prevented by pretreatment YM-09151-2 but not SCH 23390 prior to each MAP administration. The reduction of striatal TRH receptor binding was prevented by pretreatment with either antagonist. These results indicate that changes in striatal substance P level and substance P receptor binding induced by subchronic MAP treatment are mediated via activation of D-2 but not D-1 receptors by MAP-released dopamine, while changes in striatal TRH receptor binding are mediated via both D-1 and D-2 receptors.
en-copyright=
kn-copyright=

en-aut-name=OnoueTaichi
en-aut-sei=Onoue
en-aut-mei=Taichi
kn-aut-name=尾上太一
kn-aut-sei=尾上
kn-aut-mei=太一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=Methamphetamine
kn-keyword=Methamphetamine
en-keyword=Substance P
kn-keyword=Substance P
en-keyword=Thyrotropin-releasing hormone
kn-keyword=Thyrotropin-releasing hormone
en-keyword=SCH 23390
kn-keyword=SCH 23390
en-keyword=YM-09151-2
kn-keyword=YM-09151-2
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=3-4
article-no=
start-page=485
end-page=495
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199004
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Regional distribution of tyrosine, tryptophan and their metabobites in the brain of E1 mice
kn-title=E1マウス脳内チロシンおよびトリプトファンならびに関連代謝産物の局所的変動に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The contents of tyrosine (Tyr), tryptophan (Trp) and their metabolites in brain regions of ddY, non-stimulated E1 (E1 (-)) and stimulated E1 (E1 (+)) mice were measured using a Three Dimensional HPLC System. In the cerebral cortex, striatum, midbrain and cerebellum, Trp contents of E1 (+) mice were higher than those of ddY and E1 (-) mice. The contents of 5-hydroxytryptophan in E1 (-) or (+) mice brain were lower than those in ddY mice except in the medulla oblongata. Those in the cerebral cortex, and midbrain of E1 (+) mice were lowest. Brain regional serotonin (5-HT) contents of E1 (+) mice seemed to be slightly higher than those of ddY and E1 (-) mice. In the cerebral cortex, hippocampus, medulla oblongata and cerebellum of E1 (+) or (-) mice, the kynurenin contents were remarkably high compared to ddY mice. Although brain Tyr content did not differ between the three groups, the dopamine contents in the cerebral cortex, hypothalamus and striatum of E1 (+) mice were lower than those in ddY mice, and those in the cerebral cortex and striatum of E1 (+) mice were higher than those in E1 (-) mice. The norepinephrine contents did not differ between E1 (-) and ddY mice, but some brain regions of E1 (+) mice had higher levels. The content of 3-methoxy-4-hydroxyphenylglycol of E1 (-) mice was lower, and in E1 (+) mice was lowest in 7 brain regions. The tyramine contents in E1 (-) or (+) mice brains were higher than those in ddY mice, except in the midbrain of E1 (+) mice. These data, suggest a possible genetic metabolic abnormality of Try and Tyr in the brains of E1 mice.
en-copyright=
kn-copyright=

en-aut-name=SuzukiShigeki
en-aut-sei=Suzuki
en-aut-mei=Shigeki
kn-aut-name=鈴木茂樹
kn-aut-sei=鈴木
kn-aut-mei=茂樹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=tyrosine
kn-keyword=tyrosine
en-keyword=tryptophan
kn-keyword=tryptophan
en-keyword=5-hydroxytryptophan
kn-keyword=5-hydroxytryptophan
en-keyword=serotonin
kn-keyword=serotonin
en-keyword=kynurenine
kn-keyword=kynurenine
en-keyword=regional distribution
kn-keyword=regional distribution
END

start-ver=1.4
cd-journal=joma
no-vol=37
cd-vols=
no-issue=3
article-no=
start-page=179
end-page=191
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1983
dt-pub=198306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characteristics of muscarinic acetylcholine receptors in rat brain.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Characteristics of muscarinic acetylcholine (ACh) receptors were studied in the rat central nervous system (CNS) using 3H-quinuclidinyl benzilate (QNB), an antagonist of muscarinic ACh receptors. Scatchard analysis indicated that the rat CNS had a single 3H-QNB binding site with an apparent dissociation constant (Kd) of 5.0 X 10(-10) M. Li+, Zn++ and Cu++ had strong effects on 3H-QNB binding which indicates that these metal ions might play important roles at muscarinic ACh receptor sites in the brain. Since antidepressants and antischizophrenic drugs displaced the binding of 3H-QNB, the anticholinergic effects of these drugs need to be taken into account when they are applied clinically. The muscarinic ACh receptor was successfully solubilized with lysophosphatidylcholine. By gel chromatography, with a Sepharose 6B column, the solubilized muscarinic ACh receptor molecule eluted at the fraction corresponding to a Stokes' radius of 6.1 nm. With the use of sucrose-density-gradient centrifugation, the molecular weight of the solubilized muscarinic ACh receptor was determined to be about 90,000 daltons. The regional distribution of 3H-QNB binding in rat brain was examined, and the highest level of 3H-QNB binding was found to be in the striatum followed by cerebral cortex and hippocampus, indicating that muscarinic ACh mechanisms affect CNS function mainly through these areas.</p>

en-copyright=
kn-copyright=

en-aut-name=NukinaItaru
en-aut-sei=Nukina
en-aut-mei=Itaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University
en-keyword=muscarinic acetylcholine receptors
kn-keyword=muscarinic acetylcholine receptors
en-keyword=central nervous system
kn-keyword=central nervous system
en-keyword=ion effect
kn-keyword=ion effect
en-keyword=solubilization
kn-keyword=solubilization
en-keyword=molecular weight
kn-keyword=molecular weight
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=4
article-no=
start-page=201
end-page=208
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The effect of acute and repeated ethanol administration on monoamines and their metabolites in brain regions of rats.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Concentrations of norepinephrine (NE), dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were determined in eleven brain regions of rats following acute and repeated ethanol administration: (a) an intraperitoneal (i.p.) injection of 1, 2, 3 or 4g ethanol/kg body weight and (b) i.p. injection of 1 or 2g ethanol/kg body weight for seven consecutive days. After acute administration, the concentrations of monoamines and their metabolites appeared to be altered in all brain regions examined except substantia nigra and dorsal amygdala, with maximal variation 2 or 3h after 3g ethanol administration. After repeated administration, the alterations following injections of 2.0g/kg were more marked than the injections of 1.0g/kg. Generally, the levels of NE, DA and 5-HT were decreased while the levels of HVA, DOPAC and 5-HIAA were increased with a few exception. The most prominent findings were seen in the striatum, nucleus accumbens and locus coeruleus. These data indicate that concentrations of monoamines and their metabolites can be determined simultaneously in discrete brain regions and that monoaminergic systems in the brain respond region-specifically to ethanol treatment.&#60;/P&#62;</p>

en-copyright=
kn-copyright=

en-aut-name=KaneyukiTakao
en-aut-sei=Kaneyuki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MorimasaTadaomi
en-aut-sei=Morimasa
en-aut-mei=Tadaomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkadaHidetosi
en-aut-sei=Okada
en-aut-mei=Hidetosi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=shohmoriToshikiyo
en-aut-sei=shohmori
en-aut-mei=Toshikiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama&#12288;Prefectural&#12288;Junior&#12288;College&#12288;

affil-num=2
en-affil=
kn-affil=Okayama&#12288;University

affil-num=3
en-affil=
kn-affil=Okayama&#12288;University

affil-num=4
en-affil=
kn-affil=Okayama niversity
en-keyword=ethanol
kn-keyword=ethanol
en-keyword=dopamine
kn-keyword=dopamine
en-keyword=norepinephrine
kn-keyword=norepinephrine
en-keyword=serotonin
kn-keyword=serotonin
en-keyword=striatum
kn-keyword=striatum
END

start-ver=1.4
cd-journal=joma
no-vol=59
cd-vols=
no-issue=4
article-no=
start-page=135
end-page=143
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=200508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vascular changes in the rat brain during chronic hypoxia in the presence and absence of hypercapnia.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Changes in brain vascularity in adult rats during adaptation to chronic normobaric hypoxia with or without elevated CO(2) were morphometrically investigated. Immunohistochemistry with anti-rat endothelial cell antigen (RECA-1) antibody was carried out for the vascular analysis. After the rats were subjected to hypoxia for 2 to 8 weeks (wks)(10 percent O(2) in N(2)), the total area of blood vessels was measured in 6 brain regions. After 2 wks of hypoxia, the blood vessel area was found to be significantly increased in the frontal cortex, striatum, hippocampus, thalamus, cerebellum, and medulla oblongata, by 44% , 96% , 65% , 50% , 102% and 97% , respectively. The ratio of large vessels with an area &#62; 500 micro m(2) was also increased in all brain regions. Hypoxic adaptation in brain vascularity did not change during 8 wks of hypoxia, and the hypoxia-induced levels measured in the vasculature returned to control levels 2 wks after the termination of hypoxia in areas of the brain other than the cortex and thalamus. In addition, hypoxia-induced changes in terms of the total vascular area and vessel size distribution were significantly inhibited by the elevation in CO(2), whereas chronic hypercapnia without hypoxia had no effect on brain vascularity. These findings suggested that adaptations in brain vascularity in response to hypoxia are rapidly induced, and there are regional differences in the reversibility of such vascular changes. Carbon dioxide is a potent suppressor of hypoxia-induced vascular changes, and may play an important role in vascular remodeling during the process of adaptation to chronic hypoxia.</p>

en-copyright=
kn-copyright=

en-aut-name=MiyamotoOsamu
en-aut-sei=Miyamoto
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Sumitanikazunori
en-aut-sei=Sumitani
en-aut-mei=kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiMasaru
en-aut-sei=Takahashi
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HirakawaHaruhisa
en-aut-sei=Hirakawa
en-aut-mei=Haruhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KusakabeTatsumi
en-aut-sei=Kusakabe
en-aut-mei=Tatsumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HayashidaYoshiaki
en-aut-sei=Hayashida
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItanoToshifumi
en-aut-sei=Itano
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Kagawa University, Kagawa

affil-num=2
en-affil=
kn-affil=Kagawa University

affil-num=3
en-affil=
kn-affil=Kagawa University

affil-num=4
en-affil=
kn-affil=National Defense Medical College, Saitama

affil-num=5
en-affil=
kn-affil=&#65279;Kokushikan University	 

affil-num=6
en-affil=
kn-affil=International Buddhist University, Osaka

affil-num=7
en-affil=
kn-affil=Kagawa University
en-keyword=hypoxic adaptation
kn-keyword=hypoxic adaptation
en-keyword=brain vascularity
kn-keyword=brain vascularity
en-keyword=anti-rat endothelial cell antigen
kn-keyword=anti-rat endothelial cell antigen
en-keyword=carbon dioxide
kn-keyword=carbon dioxide
END

start-ver=1.4
cd-journal=joma
no-vol=52
cd-vols=
no-issue=1
article-no=
start-page=49
end-page=53
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1998
dt-pub=199802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Involvement of the Central Catecholaminergic System in Nicotine-Induced Tail-Tremor in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The effect of 6-hydroxydopamine on repeated nicotine-induced tail-tremor was investigated in rats. Tail-tremor induced by nicotine (0.5 mg/kg/day, subcutaneously) became more pronounced in intensity with daily administration for 9 days. Rats pretreated with 6-hydroxydopamine (250 micrograms, intracerebroventricularly) showed almost the maximum degree of tail-tremor during the whole experimental period. However, in rats pretreated with 6-hydroxydopamine plus desipramine, enhancement of tail-tremor was slight in the beginning but increased with the daily nicotine administration. Fourteen-day administration of nicotine did not result in significant changes in noradrenaline and dopamine levels in the cortex, hypothalamus, striatum and nucleus accumbens. These results suggest that nicotine-induced tail-tremor is associated with the supersensitivity of postsynaptic catecholaminergic receptors in the central nervous system, and that the noradrenergic system may be more important than the dopaminergic system in this phenomenon.</p>

en-copyright=
kn-copyright=

en-aut-name=SuemaruKatsuya
en-aut-sei=Suemaru
en-aut-mei=Katsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawakamiYasuhiro
en-aut-sei=Kawakami
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ArakiHiroaki
en-aut-sei=Araki
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=GomitaYutaka
en-aut-sei=Gomita
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanizakiYoshiro
en-aut-sei=Tanizaki
en-aut-mei=Yoshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univeristy

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=nicotine
kn-keyword=nicotine
en-keyword=tail-tremor
kn-keyword=tail-tremor
en-keyword=6-hydroxydopamine
kn-keyword=6-hydroxydopamine
en-keyword=noradrenaline
kn-keyword=noradrenaline
en-keyword=dopamine
kn-keyword=dopamine
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=3
article-no=
start-page=153
end-page=159
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1989
dt-pub=198906
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Action of peripherally administered cholecystokinin on monoaminergic and GABAergic neurons in the rat brain.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>In an acute study, cholecystokinin octapeptide sulfate (CCK) in doses of 1, 10 or 100 micrograms/kg body weight was injected intraperitoneally into rats just prior to the dark cycle. Rats were sacrificed two hours following the CCK injection. Norepinephrine levels were elevated in the dorsal amygdala of rats injected with 10 micrograms of CCK as well as in the septum of rats injected with 1 and 10 micrograms of CCK. The dopamine level in the septum of rats injected with 1 microgram of CCK as well as the gamma-aminobutyric acid (GABA) level in the lateral hypothalamus of rats injected with 10 micrograms of CCK were also elevated. In a chronic study, CCK (1 microgram/kg body weight/h) was subcutaneously infused into rats with Alzet osmotic minipump for seven consecutive days. The daily food consumption did not change during the 7 days of CCK infusion. The dopamine turnover in the striatum accelerated and the GABA level increased. On the contrary, dopamine metabolism in the substantia nigra and locus coeruleus decreased. Furthermore, the serotonin level in the substantia nigra decreased. Norepinephrine levels decreased in the nucleus paraventricularis, the locus coeruleus and the substantia nigra. The results suggest that peripherally administered CCK may act on the monoaminergic neurons and GABAergic neurons in the brain.</p>

en-copyright=
kn-copyright=

en-aut-name=KaneyukiTakao
en-aut-sei=Kaneyuki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MorimasaTadaomi
en-aut-sei=Morimasa
en-aut-mei=Tadaomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShohmoriToshikiyo
en-aut-sei=Shohmori
en-aut-mei=Toshikiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Prefectural Junior College

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama  University
en-keyword=cholecystokinin
kn-keyword=cholecystokinin
en-keyword=nigro-striatum
kn-keyword=nigro-striatum
en-keyword=dopamine
kn-keyword=dopamine
en-keyword=serotonin
kn-keyword=serotonin
en-keyword= ?-aminobutyric acid
kn-keyword= ?-aminobutyric acid
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=8
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199002
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In Vivo Analysis of Extracellular Proteins in Rat Brains with a Newly Developed Intracerebral Microdialysis Probe
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Peptides and proteins in the extracellular space in the central nervous system were investigated in vivo using an intracerebral microdialysis probe. The molecular cut-off of the hollow fiber which was used for the probe was approximately 100 kDa. We examined recovery rates of several compounds in vitro. The recovery rates of proteins and peptides were between 7-28%, with the exceptions of substance P and insulin-like growth factor I. The recovery rates of monoamines and their metabolites were 22-40%. In in vivo studies, two major proteins with apparent molecular weights of 62 kDa and 12 kDa, and several minor proteins (28 kDa, 43 kDa, 52 kDa and 70 kDa) were detected by SDS-polyacrylamide gel electrophoresis in the dialysate from a probe implanted in the striatum of anesthetized rats. These results suggest that the newly developed, intracerebral microdialysis probe might be useful for investigating the dynamic changes of peptides and proteins in the central nervous system.</p>

en-copyright=
kn-copyright=

en-aut-name=NakamuraMitsuo
en-aut-sei=Nakamura
en-aut-mei=Mitsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ItanoToshifumi
en-aut-sei=Itano
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamaguchiFuminori
en-aut-sei=Yamaguchi
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizobuchiMasayuki
en-aut-sei=Mizobuchi
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TokudaMasaaki
en-aut-sei=Tokuda
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsuiHideki
en-aut-sei=Matsui
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EtohSiji
en-aut-sei=Etoh
en-aut-mei=Siji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HosokawaKiyoshi
en-aut-sei=Hosokawa
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OhmotoTakashi
en-aut-sei=Ohmoto
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HataseOsamu
en-aut-sei=Hatase
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Kagawa Medical School

affil-num=2
en-affil=
kn-affil=Kagawa Medical School

affil-num=3
en-affil=
kn-affil=Kagawa Medical School

affil-num=4
en-affil=
kn-affil=Kagawa Medical School

affil-num=5
en-affil=
kn-affil=Kagawa Medical School

affil-num=6
en-affil=
kn-affil=Kagawa Medical School

affil-num=7
en-affil=
kn-affil=Kagawa Medical School

affil-num=8
en-affil=
kn-affil=Kagawa Medical School

affil-num=9
en-affil=
kn-affil=Kagawa Medical School

affil-num=10
en-affil=
kn-affil=Kagawa Medical School
en-keyword=protein
kn-keyword=protein
en-keyword=peptide
kn-keyword=peptide
en-keyword=microdialysis
kn-keyword=microdialysis
en-keyword=extracellular space
kn-keyword=extracellular space
en-keyword=probe
kn-keyword=probe
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=1
article-no=
start-page=13
end-page=17
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=199502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurotransmitter interactions in the striatum and hypothalamus of mice after single and repeated ethanol treatment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>In single treatment study, ethanol was administered intraperitoneally to ICR mice (about 34 g) in the amounts of 1.0, 2.0, 3.0 or 4.0 g/kg body weight. The 3,4-dihydroxyphenylacetic acid (DOPAC) + homovanillic acid (HVA) concentration in the striatum was elevated with 3.0 and 4.0 g/kg of ethanol. In the hypothalamus, the DOPAC, HVA and 5-hydroxyindoleacetic acid concentrations were increased after injection of 3.0 and 4.0 g/kg of ethanol. Furthermore, the acetylcholine (ACh) and gamma-aminobutyric acid (GABA) concentrations were also increased following the injection of 1.0, 2.0, 3.0 and 4.0 g/kg. To study the effects of repeated administration, mice were injected intraperitoneally with 1.0 or 2.0 g/kg of ethanol once daily for 7 days. The DOPAC + HVA level in the striatum was elevated after injection of 1.0 and 2.0 g/kg of ethanol. The GABA and ACh concentrations in the hypothalamus were decreased after repeated injections of ethanol. These results suggest that ethanol significantly alters the utilization of dopamine, ACh and GABA in the hypothalamus. This may partially explain why ethanol has such profound effects on emotional behavior and mood.</p>

en-copyright=
kn-copyright=

en-aut-name=KaneyukiTakao
en-aut-sei=Kaneyuki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MorimasaTadaomi
en-aut-sei=Morimasa
en-aut-mei=Tadaomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShohmoriToshikiyo
en-aut-sei=Shohmori
en-aut-mei=Toshikiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Prefectural University

affil-num=2
en-affil=
kn-affil=Okayama Prefectural University

affil-num=3
en-affil=
kn-affil=Okayama Prefectural University
en-keyword=ethanol
kn-keyword=ethanol
en-keyword=dopamine
kn-keyword=dopamine
en-keyword=serotonin
kn-keyword=serotonin
en-keyword= ?-aminobutyric acid
kn-keyword= ?-aminobutyric acid
en-keyword=acetylcholine
kn-keyword=acetylcholine
en-keyword=striatum
kn-keyword=striatum
en-keyword=hypothalamus
kn-keyword=hypothalamus
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=2
article-no=
start-page=93
end-page=99
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1984
dt-pub=198404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Influence of liver injury on the catecholamine metabolism in rat brain.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The present study investigated the brain catecholamine metabolism of rats with liver injury induced either by malnutrition or with CCl4. In the malnutrition group, the plasma tyrosine concentration was low, while it showed a tendency to be high in the cerebral cortex. Dopamine concentrations were low in both the cerebral cortex and diencephalon. Norepinephrine concentrations were low in the cerebral cortex, striatum and diencephalon. Tyrosine hydroxylase activity was elevated while monoamine oxidase activity was decreased in the striatum. In the CCl4 group, tyrosine concentrations in the plasma and cerebral cortex did not change. The dopamine concentration in the cerebral cortex increased five days after, and the norepinephrine concentration in the diencephalon increased 24 h after the last administration of CCl4. These data suggest that catecholaminergic neurons in the brain may be substantially affected by liver injury. It may be considered that malnutrition disturbs brain development, particularly in young rats.</p>

en-copyright=
kn-copyright=

en-aut-name=KaneyukiTakao
en-aut-sei=Kaneyuki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShohmoriToshikiyo
en-aut-sei=Shohmori
en-aut-mei=Toshikiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University
en-keyword=brain
kn-keyword=brain
en-keyword=catecholamine
kn-keyword=catecholamine
en-keyword=malnutrition
kn-keyword=malnutrition
en-keyword=carbon tetrachloride
kn-keyword=carbon tetrachloride
en-keyword=liver injury
kn-keyword=liver injury
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=4
article-no=
start-page=403
end-page=407
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1984
dt-pub=198408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Relationship of tyrosine concentration to catecholamine levels in rat brain.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Rats were fed a choline-free low protein diet for 12 or 26 weeks. In the 12-week group, the brain tyrosine concentration did not change. Dopamine levels were low in both the cerebral cortex and striatum. Norepinephrine level was low in the diencephalon. In the 26-week group, the tyrosine concentration was high in the brain. However, the dopamine and norepinephrine levels did not change in the cerebral cortex, striatum and hypothalamus. Furthermore, in another group of rats which were intraperitoneally injected with tyrosine, the brain tyrosine concentration was high, whereas the dopamine and norepinephrine levels in the hypothalamus were not significantly different from control levels.</p>

en-copyright=
kn-copyright=

en-aut-name=KaneyukiTakao
en-aut-sei=Kaneyuki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MorimasaTadaomi
en-aut-sei=Morimasa
en-aut-mei=Tadaomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShohmoriToshikiyo
en-aut-sei=Shohmori
en-aut-mei=Toshikiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University
en-keyword=brain tyrosine
kn-keyword=brain tyrosine
en-keyword=catecholamine
kn-keyword=catecholamine
en-keyword=malnutrition
kn-keyword=malnutrition
en-keyword=liver injury
kn-keyword=liver injury
END

start-ver=1.4
cd-journal=joma
no-vol=89
cd-vols=
no-issue=9-10
article-no=
start-page=1137
end-page=1149
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1977
dt-pub=19771030
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Fluorescence and electron microscopic studies of corpus striatum of the brain
kn-title=線条体の蛍光顕微鏡的,電子顕微鏡的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The distribution of catecholamine in corpus striatum, especially in caput nuclei caudati, was investigated by Falck-Hillarp method using several mammals (monkey, goat, dog, cat, rabbit, guinea pig, rat and mouse). The fluorescence of catecholamine was not observed in large and small nerve cells and bundles of myelinated nerve fibers in this nucleus of all animals used, but diffuse fluorescence was shown in neuropil (which consisted of myelinated and non-myelinated nerve fibers, dendrites of nerve cells and processes of glia cells) between these cell bodies. The ultrastructure of caput nuclei caudati of dog was also observed with electron microscopy. Intracellular organella were highly developed in large nerve cells, but not in small cells in this nucleus. Many synapses were observed in neuropil and these presynaptic fibers ended to postsynaptic fibers without large terminal boutons. These synapses were type 1 and 2 described by Gray. These results suggest that the sites where strong fluorescence showed in caput nuclei caudati of all mammals corresponded to the sites where many synapses existed, and that catecholamine was involved in nerve endings in these synapses.
en-copyright=
kn-copyright=

en-aut-name=ShobatakeHisayuki
en-aut-sei=Shobatake
en-aut-mei=Hisayuki
kn-aut-name=正畠久之
kn-aut-sei=正畠
kn-aut-mei=久之
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一解剖学教室
END

start-ver=1.4
cd-journal=joma
no-vol=91
cd-vols=
no-issue=11-12
article-no=
start-page=1507
end-page=1525
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1979
dt-pub=19791230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An electroencephalographic study on Creutzfeldt-Jakob disease- Report of two autopsy cases and literature review
kn-title=Creutzfeldt-Jakob病の脳波学的検討 ―2剖検例の報告と文献的考察―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This report concerns 2 autopsy cases of Creutzfeldt-Jakob disease (CJD) in which the relationship between changes in serial electroencephalograms and the course of the disease is analysed. The importance of timing when periodic synchronous discharge (PSD) occurs was indicated. i.e., the appearance of PSD paralleled clinical manifestations of the apallic syndrome and was most distinct when the disease was at its worst. We reviewed the EEG findings in autopsy cases of CJD reported in Japan. Fifteen cases of typical PSD were found and these were examined clinico-pathologically. The findings were: 1. PSD was recorded within three months of the onset of the disease in two thirds of the 15 cases. 2. In 13 cases the clinical manifestations when PSD occurred were those of apallic syndrome or of similar conditions. 3. Following characteristics were found in the distribution of pathological changes in the brain; (a) The presence of extensive changes in the cerebral cortex was the only finding common to all cases. (b) The cerebral changes mainly occurred in the corpus striatum of the basal ganglia and in the medical nuclei of the thalamus. (c) Disturbances were least in the brain-stem below the level of the midbrain. (d) No definite tendency was apparent in the changes of the cerebral white matter and cerebellum. In conclusion, the mechanism of PSD may be accounted for by disturbances of the cortico-thalamic circuit. This circuit is said to be regulated by diffuse thalamic projection system. It is presumed that the extensive pathology in the cortex and medical nuclei of the thalamus plays an important role.
en-copyright=
kn-copyright=

en-aut-name=YoshinagaJunji
en-aut-sei=Yoshinaga
en-aut-mei=Junji
kn-aut-name=好永順二
kn-aut-sei=好永
kn-aut-mei=順二
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=社会保険・広島市民病院・神経科
en-keyword=Creutzfeldt-Jakob病
kn-keyword=Creutzfeldt-Jakob病
en-keyword=周期性同期性放電(PSD)
kn-keyword=周期性同期性放電(PSD)
END

start-ver=1.4
cd-journal=joma
no-vol=91
cd-vols=
no-issue=3-4
article-no=
start-page=379
end-page=396
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1979
dt-pub=19790430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Diurnal variations in motor activity and regional brain monoamine content in young adult and aged rats
kn-title=若齢成熟および老齢ラットの行動量と脳部位別モノアミン量の日内変動
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diurnal variations in motor activity and regional monoamine levels of the brain in both young adult and aged wistar male rats were compared. The young adult group (Y group) consisted of 16 week old rats. The aged group (A group) comprised 19 month old rats. All the animals were housed in a room with an alternating 12 hour dark-light cycle. The temperature was kept at 24℃ and the moisture at 55 % . Motor activity was measured in selected rats by Animex. Both groups were then subdivided into six smaller groups. The animals of these groups were sacrificed by decapitation every 4 hours of the 24 hour period (2, 6 and 10 hours in the dark cycle, and 2, 6 and 10 hours in the light cycle; D2, D6, D10, L2, L6 and L10). Immediately after decapitation, brains were collected, dissected into six different regions (amygdala [Amy], corpus striatum [St], cerebral cortex [Cor] , hippocampus [Hip], diencephalon [Die] and brain stem [B. S.]), and the levels of dopamin [DA], norepinephrine [NE] and serotonin [5-HT] in each determined fluorometrically. The results were as follows. 1. Diurnal variation of motor activity. Both Y and A groups showed a marked difference between the dark and light cycles. Activity increased during the first 4 hours of the dark cycle, then decreased gradually during the rest of the dark cycle. Motor activity decreased markedly immediately after beginning of the light cycle, and remained decreased throughout the light period. The motor activity of the both groups increased transiently a little before the light cycle. Y group activity increased directly before the dark time. A group activity was significantly less than that of Y group, except for 2 time points during the light cycle. A group motor activity was about 50 % lower than that of the Y group. 2. Diurnal variation of DA. Amy from both groups showed a higher levels in the dark time than in the light. St showed two peaks in both groups but the range of variation was wider in A group than in Y group. Cor from both groups showed a higher level in the light time than in the dark. The levels of Hip, Die and B. S. in both groups showed little variation, the range being much smaller in A group. There was no significant difference in the levels of Amy, Cor and Hip in either group, but St, Die and B. S. were significantly lower in A group throughout almost the entire 24 hour period. 3. Diurnal variation of NE levels. Marked variations in Amy, Cor, Hip and Die occurred in both groups. The NE level in the 4 brain regions tended to be lower during the dark time than during the light. The diurnal variation of amine levels in St was smaller in the groups than in the other five regions. B. S. in the Y group showed lower levels during the dark time; however, B. S. from A group showed almost constant levels during the 24 hour period. The NE levels of each groups showed little difference in brain regions other than B. S.. In A group, B. S. showed 1.8 to 9 times higher levels than Y group at all examined time points. 4. Diurnal variation in 5-HT levels. Both groups showed higher amine levels in Amy, Hip and Die during the dark period than in the light. St in Y group showed two peaks at D10 and L6 but the same region in A group showed almost constant amine levels during the diurnal period except for D6. The level in Cor from both groups showed little variation, the range being much smaller in A group than in Y group. The level in B.S. of Y group showed a marked dark-light difference with a high peak at L2 but the same region from A group showed a gradual variation in the amine level with a peak between D10 and L2. Comparison of the 5-HT levels in Y and A groups showed that there was no significant difference in Amy, Hip and Die. The level in St remained high throughout the diurnal period in Y group. The level in Cor showed a higher value during the 24 h period in A group. The amine level in B. S. was higher in the A group at two time points of the dark period than in Y group. The data indicate a characteristic influence of aging on diurnal variations of motor activity and three monoamine contents of the brain. Some regions of the brain showed no difference in DA levels of Y and A groups, whereas other regions showed significantly lower levels in A group. Some regions showed no difference in NE levels of both groups and the other showed significantly higher levels in A group. These results suggest that the turnover rate of DA in some brain regions is accelerated in A group compared to Y group. A group tended to show less diurnal variation in the three monoamine levels of the brain than Y group when related to the reduced motor activity of A group, this suggests that metabolism of these monoamines in related to behavior.
en-copyright=
kn-copyright=

en-aut-name=DoiTohru
en-aut-sei=Doi
en-aut-mei=Tohru
kn-aut-name=土井亨
kn-aut-sei=土井
kn-aut-mei=亨
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設脳代謝神経科
en-keyword=老化
kn-keyword=老化
en-keyword=日内変動
kn-keyword=日内変動
en-keyword=運動量
kn-keyword=運動量
en-keyword=脳内モノアミン量
kn-keyword=脳内モノアミン量
en-keyword=部位別脳
kn-keyword=部位別脳
END

start-ver=1.4
cd-journal=joma
no-vol=94
cd-vols=
no-issue=3-4
article-no=
start-page=315
end-page=330
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1982
dt-pub=19820430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A study of dopamine receptors in the rat central nervous system Part 2. Regulation of dopamine receptors in the rat striatum after long-term treatment with antiparkinsonian drugs or neuroleptics.
kn-title=中枢神経系のdopamine受容体に関する研究 第2編 抗パーキンソン病薬ならびに抗精神病薬反復投与によるdopamine受容体の調節
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Long-term drug studies in animals using antiparkinsonian drugs (L-dopa and bromocriptine) and neuroleptics (chlorpromazine and haloperidol) can provide valuable clinical information on the mechanism of drug action and can contribute to a better understanding of the side effects of such therapy. Moreover, it has been suggested that the molecular action of these drugs involves dopamine receptors in the brain. Recently, it was proposed that the dopamine receptor exists in two forms: a D(1)-dopamine receptor, which is coupled to dopamine sensitive adenilate cyclase, and a D(2)-dopamine receptor, which is uncoupled. I have established D(1)-dopamine-radioreceptor assay and D(2)-dopamine-radioreceptor assay using [(3)H]-dopamine as a ligand, then I studied the effects of chronic administration of these drugs on two forms of dopamine receptors. It is well known that most patients on prolonged L-dopa therapy either become refractory to the drug, or develop "on-off" phenomena or dyskinesias. In this study, an increase in high affinity binding sites of D(1)-dopamine receptor was detected, whereas D(2)-dopamine receptor subsensitivity was observed following long-term L-dopa therapy. On the other hand, after bromocriptine treatment for 14days, the high affinity binding sites of D(1)-and D(2)-dopamine receptors were increased in the rat striatum. The finding that long-term bromocriptine therapy increases D(1)-and D(2)-dopamine receptors may explain, in part, the efficacy of combination bromocriptine and L-dopa treatment. After chlorpromazine treatment for 14 days, the high affinity binding sites of D(1)-and D(2)-dopamine receptors were slightly increased in rat striatum, and after haloperidol treatment for 14 days, the high affinity binding sites of D(2)-dopamine receptor were also slightly increased in rat striatum. Therefore, it was suggested that symptoms of extrapyramidal side effects after long-term neuroleptic treatment reflect a functional supersensitivity of dopamine receptors in the rat striatum.
en-copyright=
kn-copyright=

en-aut-name=YamawakiYasuhide
en-aut-sei=Yamawaki
en-aut-mei=Yasuhide
kn-aut-name=山脇泰秀
kn-aut-sei=山脇
kn-aut-mei=泰秀
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第三内科学講座
en-keyword=L-dopa
kn-keyword=L-dopa
en-keyword=bromocriptine
kn-keyword=bromocriptine
en-keyword=chlorpromazine
kn-keyword=chlorpromazine
en-keyword=haloperidol
kn-keyword=haloperidol
en-keyword=D(1)-dopamine受容体
kn-keyword=D(1)-dopamine受容体
en-keyword=D(2)-dopamine受容体
kn-keyword=D(2)-dopamine受容体
en-keyword=受容体のsupersensitivity
kn-keyword=受容体のsupersensitivity
END

start-ver=1.4
cd-journal=joma
no-vol=98
cd-vols=
no-issue=5-6
article-no=
start-page=439
end-page=456
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1986
dt-pub=19860630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The hitochemical changes of non-dopaminergic neurons of the mouse striatum induced by l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a nigrostriatal dopaminergic neurotoxin used for a model of Parkinson's disease.
kn-title=MPTP投与パーキンソン病モデルマウスの線条体における非ドパミン神経の組織化学的変化
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effects of MPTP on non-dopaminergic neurons were studied in the striatum of ICR mice, by means of enzyme histochemistry for neurons containing acetylcholinesterase (AChE) or NADPH(2)-diaphorase and of immunohistochemistry for neurons containing GABA, serotonin or enkephalin. The most prominent changes were observed in immunohistochemical staining for enkephalin, 3 days after the treatment with MPTP. Enkephalinimmunoreactive nerve fibers and terminals were increased both in number and in intensity, particularly at enkephalin-rich islands seen in the rostral striatum. In addition, enkephalin-positivepass-through fibers and cell bodies were also increased throughout the striatum. The highest density of these cell bodies was found in the caudal striatum. These changes in enkephalin immunoreactivity became less evident day by day, and 60 days later the staining result appeared almost the same as that in control mice. In contrast, serotonin-immunoreactive nerve fibers became sparse, particularly in ventrolateral parts of the striatum, from 7 days after the treatment with MPTP. Such a change was obsesved for as long as 60 days, so that it was suggested that the MPTP treatment caused irreversible degenerative changes in serotonin nerve terminals of the striatum. On the other hand, no significant change was recognized in other striatal nerons containing AChE, NADPH(2)-diaphorase or GABA. The present study indicates that some non-dopaminergic neurons, either intrinsic or extrinsic to the striatum, are affected by the MPTP treatment and therefore an important to the understanding of the etiology of Parkinson's disease.
en-copyright=
kn-copyright=

en-aut-name=HochiToshikazu
en-aut-sei=Hochi
en-aut-mei=Toshikazu
kn-aut-name=芳地俊和
kn-aut-sei=芳地
kn-aut-mei=俊和
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一解剖学教室
en-keyword=MPTP
kn-keyword=MPTP
en-keyword=線条体
kn-keyword=線条体
en-keyword=非ドーパミンニューロン
kn-keyword=非ドーパミンニューロン
en-keyword=組織化学
kn-keyword=組織化学
en-keyword=マウス
kn-keyword=マウス
END

start-ver=1.4
cd-journal=joma
no-vol=95
cd-vols=
no-issue=1-2
article-no=
start-page=167
end-page=183
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1983
dt-pub=19830228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Change in nerve terminals of rat striatum after repeated treatment with methamphetamine and haloperidol -morphometrical and electron microscopic monoaminergic histochemical study-
kn-title=メタンフェタミン及びハロペリドール慢性投与のラット線条体神経終末に及ぼす影響 ―電顕モノアミン組織化学を用いた計量形態学的研究―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In order to examine the changes in dopaminergic(DA) terminals in rat striatum after methamphetamine(MAP) and/or haloperidol(HAL) treatment, the present study was made. Twenty four rats were used and divided into a control-group, a MAP-group, a HAL-group and a HAL+MAP-group. Rats in these groups received daily intraperitoneal injections of either physiological saline(10ml/kg), MAP(4mg/kg), HAL(5mg/kg) or HAL(5mg/kg) plus MAP(4mg/kg), respectively, for 13days. The reverse tolerance phenomenon was confirmed only in the MAP-group. At 8 and 36days following the daily injection session, rats were killed. Histochemical and morphometrical examination was made on the rat striatum. The number of DA terminals per unit area decreased significantly in both the MAP-group and the HAL-group at the 8th and 36th day (p<0.001), while no change was found in the HAL+MAP-group. The number of non-DA terminals per unit area and the mean area of DA terminals did not differ significantly among the four groups. Density of synaptic vesicles in DA terminals increased significantly only in the HAL+MAP-group at the 36th day(p<0.02). At the 8th day, the number of DA synaptic vesicles per unit area decreased only in the HAL-group(p<0.005), as compared to the control group. At the 36th day, however, it decreased significantly in both the MAP-group(p<0.001) and the HAL-group(p<0.02). It was concluded that the repeated administration of a dopamine agonist and antagonist can result in a morphometrical change in the rat striatal DA terminal, and the change may be long-lasting.
en-copyright=
kn-copyright=

en-aut-name=IharaYuetsu
en-aut-sei=Ihara
en-aut-mei=Yuetsu
kn-aut-name=井原雄悦
kn-aut-sei=井原
kn-aut-mei=雄悦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=メタンフェタミン
kn-keyword=メタンフェタミン
en-keyword=ハロペリドール
kn-keyword=ハロペリドール
en-keyword=電顕組織化学
kn-keyword=電顕組織化学
en-keyword=計量形態学
kn-keyword=計量形態学
en-keyword=黒質線条体ドパミン系
kn-keyword=黒質線条体ドパミン系
END

start-ver=1.4
cd-journal=joma
no-vol=97
cd-vols=
no-issue=5-6
article-no=
start-page=515
end-page=526
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1985
dt-pub=19850630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Reverse tolerance by chronic methamphetamine and stress induced response -Behavioral and biochemical changes in response to footshock
kn-title=メタンフェタミン逆耐性とストレス負荷時の反応 ―Foot shockによる行動及び生化学的変化
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effects of repeated methamphetamine (MAP) treatment (4mg/kg per day for 14 days) on behavioral and neurochemical changes induced by footshock stress in rats were examined. The challenge by footshock was conducted 7 days after cessation of the chronic treatment. The duration of fighting behavior resulting from the footshock (2.5mA, 5Hz, 10min) was significantly longer in the MAP-treated rats than in controls. After the footshock stress, the number (Bmax) of specific [(3)H] -spiperone binding sites in the striatum decreased significantly in the MAP-treated rats. No differences were found between the MAP-treated rats and controls in the concentrations of monoamines and their metabolites in the frontal cortex, striatum and mesolimbic areas.
en-copyright=
kn-copyright=

en-aut-name=FujiwaraYutaka
en-aut-sei=Fujiwara
en-aut-mei=Yutaka
kn-aut-name=藤原豊
kn-aut-sei=藤原
kn-aut-mei=豊
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=メタンフェタミン
kn-keyword=メタンフェタミン
en-keyword=フットショックストレス
kn-keyword=フットショックストレス
en-keyword=モノアミン
kn-keyword=モノアミン
en-keyword=トリチウムスペピロン結合
kn-keyword=トリチウムスペピロン結合
en-keyword=闘争行動
kn-keyword=闘争行動
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=9-10
article-no=
start-page=1323
end-page=1332
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1987
dt-pub=19871031
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of phenytoin on convulsions and on brain 5 hydroxytryptamine and 5-hydroxyindoleacetic acid levels in El mice
kn-title=PhenytoinのElマウスに対する抗けいれん作用に関する研究 ―特にElマウスけいれん抑制機構へのセロトニン系の関与について―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Phenytoin (PHT) metabolism and brain monoamine levels were examined daily after chronic administration of 40mg/kg/day of PHT-Na into ddY mice. The blood PHT level increased remarkably the first day and then tended to decrease, attaining a transitory minimum on the third day of a 7-day experiment. The half-life of PHT after a single injection was about 12 hours, and the administration of PHT for 3 days shortened the half-life to about 6 hours. The urinary excretion of 5-(p-hydroxyphenyl)-5-phenylhydantoin tended to increase from the first day and attained a maximum on the fourth day of a 7-day experiment. Levels of 5-hydroxytryptamine (5-HT) and catecholamine in the mouse brain increased transitorily from the third to sixth day of a 14-day experiment. On the 14th day, these levels remained at the control level. Effects of PHT on convulsions and on regional levels of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in the El mouse brain were examined. PHT completely inhibited convulsions in El mice after intraperitoneal injections of 40mg/kg of PHT-Na twice a day for three days. After the injection of PHT twice a day for three days, the 5-HT level was increased in the striatum, hypothalamus, midbrain and pons-medulla oblongata, and the 5-HIAA level was increased in the cortex, hippocampus, midbrain, pons-medulla oblongata and cerebellum. These results suggest that the inhibitory effect of PHT on the convulsions may be based on the activation of the 5-HTergic neurone system in El mice.
en-copyright=
kn-copyright=

en-aut-name=MatsumotoYukiharu
en-aut-sei=Matsumoto
en-aut-mei=Yukiharu
kn-aut-name=松本幸治
kn-aut-sei=松本
kn-aut-mei=幸治
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=phenytoin
kn-keyword=phenytoin
en-keyword=blood level
kn-keyword=blood level
en-keyword=metabolism
kn-keyword=metabolism
en-keyword=El mouse
kn-keyword=El mouse
en-keyword=brain monoamines
kn-keyword=brain monoamines
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=9-10
article-no=
start-page=1071
end-page=1081
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1987
dt-pub=19871031
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Chronic effects of the Ca(++) channel blocker verapamil on monoamine release and metabolism in discrete rat brain regions: Comparison with the effects of methamphetamine and reserpine
kn-title=カルシウムチャンネル阻害剤verapamilの中枢モノアミン伝達物質の放出ならびに代謝に及ぼす作用 : methamphetamineおよびreserpineとの比較
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effects of chronic treatment with verapamil(VP) on monoamine release and metabolism in rat brain in vivo were compared with the effects of methamphetamine(MAP) and reserpine(RES). These drugs were administered to rats in drinking water for two weeks. The contents of monoamines (DA and 5HT) and their major metabolites(DOPAC, HVA and 5HIAA) in eight discrete brain regions were measured by HPLC-ECD. After treatment with VP, DA levels decreased in the nucleus accumbens(N.ACC) and the suprachiasmatic nucleus(SCN), but no significant changes were demonstrated in the metabolites(DOPAC, HVA). 5HT levels decreased in the N.ACC, SCN and amygdara(AMY), and 5HIAA levels decreased in the raphe dorsalis(RD). GABA contents were increased in the N.ACC. After treatment with MAP, DA levels decreased in the N.ACC, striatum(STR) and ventro-medial hypothalamic regions(VMH). No significant change was shown in the metabolites. 5HT contents decreased in the N.ACC, STR, AMY, VMH and RD. 5HIAA contents decreased significantly in the RD. After treatment with RES, DA levels decreased in the N.ACC, STR and SCN. HVA contents decreased in the N.ACC and SCN, though they increased in the LH and SN. 5HT levels decreased in the N.ACC, SCN, AMY and RD. High 5HIAA concentrations were found in the N.ACC, STR, LH and VMH. DA, DOPAC and HVA levels were reduced more in several regions by co-administration of VP and MAP than by MAP treatment alone. DA was lowered more in the RD and HVA was lowered more in several regions by co-administration of VP and RES than by RES treatment alone. The well known locomotor hyperactivity induced by MAP was enhanced by VP. The present study suggests that there are at least two classes of voltage-gated calcium channels in the central nervous system related to the release of monioamines, one sensitive to VP and other not. In addition, chronic VP treatment may have an inhibitory effect on the release and synthesis of monoamines.
en-copyright=
kn-copyright=

en-aut-name=IkedaMasaaki
en-aut-sei=Ikeda
en-aut-mei=Masaaki
kn-aut-name=池田正明
kn-aut-sei=池田
kn-aut-mei=正明
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設病態生化学部門
en-keyword=Verapamil
kn-keyword=Verapamil
en-keyword=Ca(2+)-channel
kn-keyword=Ca(2+)-channel
en-keyword=Methamphetamine
kn-keyword=Methamphetamine
en-keyword=Reserpine
kn-keyword=Reserpine
en-keyword=Monoamine release
kn-keyword=Monoamine release
END

start-ver=1.4
cd-journal=joma
no-vol=100
cd-vols=
no-issue=7-8
article-no=
start-page=721
end-page=741
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=1988
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Vestibulo-thalamic projections and head posture in the cat.
kn-title=ネコの前庭視床投射と頭位変化に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The vestibulo-thalamic projections were studied using the retrograde axonal transport technique by injection of horseradish peroxidase (HRP) into the unilateral ventrolateral (VL) thalamic nucleus in 12 cats. The results of experiments in which HRP was injected into the VL-thalamus, including the dorsomedial and central lateral thalamic nuclei, of two cats suggest that major inputs to the thalamus arise predominantly from the contralateral superior nucleus and ipsilateral medial and lateral vestibular nuclei.The functional significance of the connections was studied in 15 cats by eliciting head postures such as turning, tilting or a combined form following electrical stimulation of vestibular nuclei. Horizontal turning toward the ipsilateral side was evoked by stimulation of unilateral medial and lateral vestibular nuclei, and it was abolished by bilateral thalamotomy. The turning posture was also eliminated by producing a lesion in the VL-thalamus, the field of Forel H(1) and zona incerta in the contralateral side to the vestibular nuclear stimulation. However, a lesion in the same structure on the ipsilateral side made the posture worse. Therefore, it is concluded that horizontal turning of the head toward the ipsilateral side is caused by the activation of both ipsilateral vestibulo-reticulo-thalamic projections and contralateral vestibulo-thalamo-striate projections.Lateral tilting of the head toward the contralateral side was evoked by stimulation of the superior vestibular nucleus or by producing a lesion in the mesencephalic ventromedial tegmentum including the interstitial nucleus of Cajal. The effect of thalamotomy on the tilting was slight, and the posture was maintained after bilateral thalamotomy. These results suggest that lateral tilting toward the contralateral side of vestibular nuclear stimulation is caused to some extent by the activation of contralateral reticulo-thalamic projections, but that it is primarily related to descending projections from the striatum and mesencephalic ventromedial tegmentum.
en-copyright=
kn-copyright=

en-aut-name=MinoShogo
en-aut-sei=Mino
en-aut-mei=Shogo
kn-aut-name=三野章呉
kn-aut-sei=三野
kn-aut-mei=章呉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳神経外科教室
en-keyword=vestibulo-thalamic projection
kn-keyword=vestibulo-thalamic projection
en-keyword=horseradish peroxidase
kn-keyword=horseradish peroxidase
en-keyword=head posture
kn-keyword=head posture
en-keyword=spasmodic torticollis
kn-keyword=spasmodic torticollis
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=7-8
article-no=
start-page=787
end-page=806
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1987
dt-pub=19870830
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Guanidino compounds in iron-induced epileptogenic foci of rats
kn-title=鉄塩誘導てんかん原性焦点組織におけるグアニジノ化合物の変動に関する研究 ― 特にラジカル反応によるグアニジノ化合物の生成について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Changes in the levels of guanidino compounds in the cortex, hippocampus, striatum, hypothalamus, midbrain, pons and medulla oblongata and cerebellum were analyzed by high performance liquid chromatography after an injection of ferric chloride into the sensory motor cortex of SD rats. Levels of guanidinoacetic acid (GAA) and methylguanidine (MG) changed greatly 15 and 30 min after the injection, but recovered to normal levels 24 to 48 hours after the injection. GAA and MG increased two or three times the normal level 2 months after the injection, at which time iron-induced epileptogenic foci were formed. Levels of other guanidino compounds, i.e., N-acetylarginine, guanidinoacetic acid, arginine (Arg), homoarginine and creatinine (CRN) also changed, though the extent of the changes was not as marked as with GAA and MG. Rapidly increased generation of hydroxyl radical and peroxide intermediate radical(s) was observed by electron spin resonance analysis after addition of ferric chloride and hydrogen peroxide to rat brain homogenate. Levels of MG and GAA also increased. A significant relationship between the generation of hydroxyl radical and the formation of MG was recognized. The formation of MG in the system was dependent on the concentration of CRN but independent of the concentration of Arg and GAA. These results suggest that MG formed from CRN may act on neurones after iron injection into the rat brain, thus forming epileptogenic feci.
en-copyright=
kn-copyright=

en-aut-name=FukushimaMasato
en-aut-sei=Fukushima
en-aut-mei=Masato
kn-aut-name=福島正登
kn-aut-sei=福島
kn-aut-mei=正登
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=鉄塩誘導てんかん原性焦点
kn-keyword=鉄塩誘導てんかん原性焦点
en-keyword=グアニジノ化合物
kn-keyword=グアニジノ化合物
en-keyword=ラット
kn-keyword=ラット
en-keyword=ラジカル反応
kn-keyword=ラジカル反応
en-keyword=メチルグアニジン
kn-keyword=メチルグアニジン
END

start-ver=1.4
cd-journal=joma
no-vol=100
cd-vols=
no-issue=5-6
article-no=
start-page=473
end-page=482
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=1988
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Determination of phenylacetic acid in the rat brain by gas chromatography/negative ion chemical ionization mass spectrometry
kn-title=ガスクロマトグラフィー／陰イオン化学イオン化質量分析法によるラット脳内フェニル酢酸の定量
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A method coupling gas chromatography/negative ion chemical ionization mass spectrometry (GC/NCI/MS) with a rapid one-step purification on a Sephadex G-10 column was developed to measure free phenylacetic acid(PAA), the major metabolite of ,β-phenylethylamine (PEA), in small amounts of the rat brain. Recovery of PAA for the Sephadex G-10 column was 96.2±2.0%.Pentafluorobenzyl derivatives of PAA (PAA-PFB) and heptadeuterated PAA (PAA-d(7)-PFB) were determined by GC/NCI/MS. No interfering peaks were present on the mass fragmentogram. A calibration curve constructed from the observed peak area ratio of PAA-PFB to PAA-d(7)-PFB and known weight ratio was linear within the range of 1.25 to 40pg PAA, with a correlation coefficient of more than 0.999. In the rat striatum, PAA was determined with 'within batch' and 'between batches' coefficients of variation of 0.81% and 1.24%, respectively.While PAA was significantly decreased by 40% of controls following treatment with pargyline,the monoamine oxidase inhibitor, a remarkable increase in the metabolite level was found following treatment with PEA. Acute and chronic treatment with antidepressants had no significant effects on PAA levels in the rat striatum. The present method should be useful in future investigations of the functional role of PEA in the brain.
en-copyright=
kn-copyright=

en-aut-name=KawabataMasahiro
en-aut-sei=Kawabata
en-aut-mei=Masahiro
kn-aut-name=川端昌弘
kn-aut-sei=川端
kn-aut-mei=昌弘
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設病態生化学部門
en-keyword=フェニル酢酸
kn-keyword=フェニル酢酸
en-keyword=ガスクロマトグラフィー／陰イオン化学イオン化質量分析法
kn-keyword=ガスクロマトグラフィー／陰イオン化学イオン化質量分析法
en-keyword=セファデックスG-10
kn-keyword=セファデックスG-10
en-keyword=抗うつ薬
kn-keyword=抗うつ薬
en-keyword=βーフェニルエチルアミン
kn-keyword=βーフェニルエチルアミン
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=1-2
article-no=
start-page=153
end-page=164
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199002
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Changes in dopamine D-1 and D-2 receptors in the rat striatum after long term treatment with haloperidol-Comparison among intermittent, continuous and very long term treatment
kn-title=ハロペリドール長期投与後のラット線条体 D-1・D-2 受容体の変化―間欠投与・持続投与・超長期時持続投与の比較―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effects of long-term treatment with haloperidol (2mg/kg/day) on dopamine receptors in the rat striatum was examined using in vitro quantitative autoradiography. Rats treated with haloperidol showed an increase in striatal D-2 receptor binding as revealed by [(3)H] spiperone. Striatal D-1 receptos labeled with [(3)H] SCH 23390 were not changed following treatment with haloperidol in young rats for 2 weeks, while, it was decreased following 85 weeks of tretment. The striatal D-1 receptors were decreased also after a 4 week treatment with haloperidot in aged rats. These results suggest that haloperidol treatment in the aged rats results in D-2 receptor supersensitivity and a decline in D-1 receptors. Such relative supersensitivity of the D-2 receptor over the D-1 receptor may be related to the vulnerability to tardive dyskinesia of the aged.
en-copyright=
kn-copyright=

en-aut-name=NishikawaHiroshi
en-aut-sei=Nishikawa
en-aut-mei=Hiroshi
kn-aut-name=西川浩
kn-aut-sei=西川
kn-aut-mei=浩
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=dopamine receptors
kn-keyword=dopamine receptors
en-keyword=haloperidol
kn-keyword=haloperidol
en-keyword=aging
kn-keyword=aging
en-keyword=striatum
kn-keyword=striatum
en-keyword=tardive dyskinesia
kn-keyword=tardive dyskinesia
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=1-2
article-no=
start-page=129
end-page=141
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199002
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Biochemical changes in the rat brain in the chronic stage after transient forebrain ischemia
kn-title=一過性虚血後の慢性期ラット脳における生化学的変化に検する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In recent years, cases of sequelae of cerebrovascular disease such as vascular dementia due to death of many neurons have been increasing. Such neuronal death following brain ischemia had been considerd to be due to an energy deficiency resulting from an impaired respiratory chain. However, the detection of the delayed neuronal death showed that neuronal death is not caused by mere energy deficiency. Most previous studies on delayed neuronal death focused on the changes in morphology and energy metabolism in the acute to subacutte stage. There are few reports concerning biochemical changes in the chronic stage, especially in neurotransmitter receptors. Transient ischemia for 20 minutes in a rat four-vessel occlusion model was induced, and serial histological and biochemical changes were evaluated until the chronic stage. Destruction of pyramidal cells in the CAI area of the hippocampus was completed by 10 days after cerebral ischemia followed by recirculation of cerebral blood flow. Light microscopy showed no progression after this day. The level of acetylcholine (ACh) was significantly decreased in the hippocampus, striatum, and frontal cortex at the termination of ischemia but recovered to normal 21 days after recirculation of cerebral blood flow. The binding sites of muscarinic ACh receptors (mACh-R) per usit of protein were increased in the hippocampus 21 days after recirculation of blood flow. However, no changes were observed in the total number of mACh-R in the entire hippocampus. Thuse finings suggest no changes in the ACh neuronal system in the chronic stage and no direct association between this ayatem and delayed neuronal death. On the other hand, N-methyl-D-aspartate (NMDA) receptors, a subtype of glutamate receptirs, showed no change in the hippocampus until after 10 days, but decreased to half after 21 days despite no evidence of histological progression of neuronal death. Thus, delayed neuronal death after transient forebrain ischemia appears to be deu to release of glutamate, an excitatory amino acid. Our findingd show the specific death of neurons with NMDA receptors for glutamate.
en-copyright=
kn-copyright=

en-aut-name=YoshikawaHiroshi
en-aut-sei=Yoshikawa
en-aut-mei=Hiroshi
kn-aut-name=吉川寛
kn-aut-sei=吉川
kn-aut-mei=寛
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=ischemia
kn-keyword=ischemia
en-keyword=acetylcholine
kn-keyword=acetylcholine
en-keyword=muscarinic acetylcholine receptor
kn-keyword=muscarinic acetylcholine receptor
en-keyword=N-methyl-D-aspartate (NMDA) receptor
kn-keyword=N-methyl-D-aspartate (NMDA) receptor
en-keyword=delayed neuronal death
kn-keyword=delayed neuronal death
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=4
article-no=
start-page=281
end-page=292
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Pharmacological specificity of antipsychotic, antiischemic and some other drugs for σ receptors labeled with [(3)H] haloperidol
kn-title=ラット脳内 σ 受容体の薬理学的特異性に関する研究―とくに抗精神病薬との抗虚血剤の作用について―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pharmacological specificity of several classes of drugs such as antipsychotics and antiischemic agents was assessed for σ receptors labeled with [(3)H] haloperidol. Specific binding of [(3)H] haloperidol in the presence of 25 nM spiperone was saturable and high affinity )Kd=1.96±1.31 nM, Bmax=2.37±0.27pmol/mg of protein;n=8). Among the 29 antipsychotics tested in inhibition studies, bromperidol and haloperidol were the most potent inhibitors (Ki=0.9nM, 1.0nM, respectively). The conventional antipsychotics moperone, timiperone etc. and the novel promising drugs YM-09151, Y-516, BMY-14802 and remoxipride potently inhibited [(3)H] haloperidol binding with the Ki in the range of low to moderate nanomolar. On the other hand, among the other 27 drugs tested, the antispasmodics eperisone and tolperisone, the antiischemic agents ifenprodil, the Ca(2+) antagonist flunarizine and cinnarizine, and the antitussives carbetapentane, cloperastine and dextromethorphan, were especially potent inhibitors. These results, taken together with the evidence that the antiischemic agents ifenprodil and dextromethorphan antagozine NMDA responses and NMDA receptor complex is a possible site of action for neuroprotective agents, strongly suggest that σ receptors may be potential sites of action for antiischemic as well as antipsychotic drugs, i.e., σ receptors mediate the neuroprotective effects of certain antiischemic agents by affecting the NMDA receptor complex.
en-copyright=
kn-copyright=

en-aut-name=ZushiYoshifumi
en-aut-sei=Zushi
en-aut-mei=Yoshifumi
kn-aut-name=図子義文
kn-aut-sei=図子
kn-aut-mei=義文
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=sigma receptors
kn-keyword=sigma receptors
en-keyword=antipsychotics
kn-keyword=antipsychotics
en-keyword=ifenprodil
kn-keyword=ifenprodil
en-keyword=dextromethorophan
kn-keyword=dextromethorophan
en-keyword=eperisone
kn-keyword=eperisone
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=1-2
article-no=
start-page=105
end-page=116
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=1991
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Alterations of neuropeptides in MPTP-treated mouse brain
kn-title=1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)　を用いたパーキンソニズム・モデルマウスにおける脳内神経ペプチドに関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) has been shown to destroy the nigrostriatal dopaminergic  system, inducing biochemical and histopathological changes resembling Parkinson's disease. Biochemical changes, especially changes of neuropeptides were determined 1,2 or 6 weeks after MPTP treatment in various regions of the mice brain.
The dopamine (DA) concentration decreased to 22% of the control level in the striatum 1 week after MPTP treatment, but recovered to 50% of the control level 6 weeks after MPTP treatment. The decrease in the noradrenaline concentration was less than that of DA. Amine fluorescence histochemistry revealed, markedly decreased amine fluorescnece in the striatum 6 weeks after MPTP treatment, and this decrease in amine fluorescence was recovered after levodopa treatment. The results of a pole thst revealed the bradykinesia of MPTP-treated mice and it was attenuated b y levodopa and amantadine hydrochloride treatments. Among the neuropeptides tested, somatostatin (SOM) increased 1 week after MPTP treatment in the striatum and the thalamus＋midbrain but decreased 6 weeks after MPTP treatment in the striatum and the hippocampus. In the striatum the decreased SOM recovered with levodopa treatment. Thus, the SOM might be regulated by a dopaminergic system. On the other hand, in the cerebral cortex, while no changes appeared in the SOM concentration after MPTP treatment, the concentration decreased significantly with levodopa treatment. Other neuropeptides such as substance P, cholecystokinin-octapeptide and thyrotropin releasing hormone did not show any significant changes up to 6 weeks after MPTP treatment.
en-copyright=
kn-copyright=

en-aut-name=KawataMakio
en-aut-sei=Kawata
en-aut-mei=Makio
kn-aut-name=河田牧男
kn-aut-sei=河田
kn-aut-mei=牧男
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=MPTP
kn-keyword=MPTP
en-keyword=parkinsonism
kn-keyword=parkinsonism
en-keyword=neuropeptide
kn-keyword=neuropeptide
en-keyword=somatostatin
kn-keyword=somatostatin
en-keyword=levodopa
kn-keyword=levodopa
en-keyword=dementia
kn-keyword=dementia
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=5-6
article-no=
start-page=471
end-page=482
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of typtophan metabolites on brain function : Electrocorticographical study
kn-title=トリプトファン代謝産物のラット脳機能に対する影響の研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effects of tryptophan (Trp) metabolites administered into right cerebroventricle (1μmol) on the electrocorticograms (ECoG) of rats were studied to investigate the roles of Trp metabolites in the brain function. Kynurenine, anthranilic acid, and xanthurenic acid has no effect on ECoG until the end of recording 4 hours after the administration. 3-Hydroxykynurenine had a suppressive effect on the ECoG transitory, and kynurenic acid suppressed ECoG slightly. 3-Hydroxyanthranilic acid which is a metabolite of 3-hydroxykynurenine, induced spike discharges with a long latency (60-230 min after the administration). 3-Hydroxyanthranilic acid is thought to be metabolized to o-aminophenol, quinolinic acid and picolinic acid. Among the 3-hydroxyanthranilic acid metabolites, o-aminophenol induced spike discharges a few min after the administration, and the spike discharges a few min after the administrations, and the spike discharges lasted 60 min. On the other hand, quinolinic acid suppressed ECoG, and picolinic acid had no effect. These electrocorticographic findings suggest that 3- hydroxyanthranilc acid might induce spike discharges after metabolization to o-aminophenol.
en-copyright=
kn-copyright=

en-aut-name=NishijimaYutaka
en-aut-sei=Nishijima
en-aut-mei=Yutaka
kn-aut-name=西嶋寛
kn-aut-sei=西嶋
kn-aut-mei=寛
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学歯学部口腔外科学第一講座
en-keyword=kynurenic acid
kn-keyword=kynurenic acid
en-keyword=3-hydroxyanthranilic acid
kn-keyword=3-hydroxyanthranilic acid
en-keyword=o-aminophenol
kn-keyword=o-aminophenol
en-keyword=quinolinic acid
kn-keyword=quinolinic acid
en-keyword=experimental seizures
kn-keyword=experimental seizures
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=7-8
article-no=
start-page=1005
end-page=1012
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Pharmacological interaction between serotonin(2) and α(2)-adrenergic receptors in the human platelet aggregation
kn-title=ヒト血小板凝集能におけるセロトニン(2)およびアルファ(2)-アドレナージック受容体の薬理学的相互作用
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To investigate the interaction between serotonin (5HT)(2) and α(2)-adrenergic receptors in the human platelet membrane, the inhibitory effects of calcium (Ca) antagonists, 5HT(2) antagonists, α(2) antagonists and adenosine (AE) receptor (A(2)) agonists on 5HT plus ADP ([5HT＋ADP]) and adrenaline (ADR) plus ADP ([ADR＋ADP])-induced washed platelet aggregation were examined. In the [5HT＋ADP] -induced aggregation. The inhibitory activity was in the order of (－)-desmethoxyverapamil (D888), mianserin (MA), ketanserin, AE>diltiazem, nicardipine, yohimbine. On the other hand, in the [ADR＋ADP] -induced aggregation, the inhibitory activity was in the order of MA, YH>D888, AE, and the rest had no significant effect even at 10 μM. Only AE among these drugs inhibited ADP-induced aggregation. The present findings indicate that the Ca antagonist D888, 5HT(2) antagonist MA and α(2) antagonist YH acted simultaneously as 5HT(2) and α(2) receptor inhibitors and imply an apparent interaction between these receptors. Since both of the aggregation responses required extracellular Ca(2+) and were modulated by Ca(2+) concentrations, the mechanism of interaction may be attributed to intracellular Ca(2+)-signaling systems.
en-copyright=
kn-copyright=

en-aut-name=OkadaHidetoshi
en-aut-sei=Okada
en-aut-mei=Hidetoshi
kn-aut-name=岡田英俊
kn-aut-sei=岡田
kn-aut-mei=英俊
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設病態生化学部門
en-keyword=platelet aggregation
kn-keyword=platelet aggregation
en-keyword=serotonin(2) receptors
kn-keyword=serotonin(2) receptors
en-keyword=α(2)-adrenergic receptors
kn-keyword=α(2)-adrenergic receptors
en-keyword=calcium antagonists
kn-keyword=calcium antagonists
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=7-8
article-no=
start-page=951
end-page=962
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The cyclic AMP-generating system of cobalt-induced epileptic cerebral cortex
kn-title=コバルト誘導てんかん性大脳皮質のサイクリック AMP 合成系に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A cobalt chloride solution was injected into the unilateral sensorimotor cortex of rats to induce epileptic activity. The cyclic AMP contents of slices incubated with or without adenosine and 2-chloroadenosine were determined in four cortical areas after electroencephalography and behavioral examination in cobalt-injected rats. Electrographic spike activity appeared immediately after injection of cobalt. In the majority of cobalt-injected rats, the spike activity was dominant in the primary epileptic region of the cortex. The spike frequency reached a maximum level two to three weeks after the injection and declined thereafter. The electrographic activity was followed by abnormal behavior. Adenosine and 2-chloroadenosine elevated the cyclic AMP levels in the cortical slices 6-to 10-fold and 10-to 16-fold, respectively. The elicitation of cyclic AMP accumulation was strongly inhibited by the adenosine antagonist 8-phenyltheophylline. The cyclic AMP accumulation elicited by adenosine or 2-chloroadenosine was increased in the primary cortical area of cobalt-induced epilepsy, but in the other cortical areas there was no deviation in cyclic AMP accumulation. The increase in cyclic AMP accumulation was observed regardless of the presence or absence of the adenosine uptake inhibitor dipyridamole, phosphodiesterase inhibitor Ro 20-1724, and adenosine deaminase. The increased accumulation of cyclic AMP in the primary epileptic cortex was detected as early as 8 days after the injection. The cyclic AMP accumulation slightly increased thereafter. It reached a plateau 17 to 19 days after the injection and then turned to the control levels, in harmony with the electrographic and behavioral profiles. These findings suggest that alterations in adenosine-sensitive generation of cyclic AMP in the primary epileptic region of the cortex are part of the neurochemical process of cobalt-induced epilepsy.
en-copyright=
kn-copyright=

en-aut-name=AsakiHideki
en-aut-sei=Asaki
en-aut-mei=Hideki
kn-aut-name=浅木秀樹
kn-aut-sei=浅木
kn-aut-mei=秀樹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一生理学教室
en-keyword=サイクリック AMP
kn-keyword=サイクリック AMP
en-keyword=アデノシン
kn-keyword=アデノシン
en-keyword=2 - クロロアデノシン
kn-keyword=2 - クロロアデノシン
en-keyword=コバルト誘導てんかん
kn-keyword=コバルト誘導てんかん
en-keyword=ラット大脳皮質
kn-keyword=ラット大脳皮質
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=7-8
article-no=
start-page=927
end-page=943
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Neuropathological study on neuronal swelling degeneration in the substantia nigra of Olivo-Ponto-Cerebellar Atrophy (OPCA)
kn-title=Olivo-Ponto-Cerebellar Atrophy (OPCA) の中脳黒質ニューロンの腫脹性病変について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In 6 out of 7 autopsy cases of olivopontocerebellar atrophy, we found characteristic features of neuronal swelling degeneration (abbr. NSD) in the nerve cell of the substantia nigra. NSD was classified into 4 types according to the microscopic features. The cell body of the type A NSD is much larger than the usual nerve cell, contains melanin granules, is round in shape and appears granular. This cell sometimes contains a shrunken nucleus, Marinesco body, Nissl granules and rest of melanin pigment, suggesting its origin in the degenerating melanin containing nerve cell. In type B NSD the periphery of the swollen cell body appears to be frosted glass with a Nissl Substance. A part of the type B NSD was suggested to have its origin in the nerve cell which has no melanin pigment. Type C NSD is round or irregular in shape and appears to be vacuolar, suggesting its origin in the dendritic process. Type D NSD is sharply bounded from the surrounding tissue and amorphous structures. Judging from its staining characteristics, its origin was suggested to be in the axon. The significance and pathogenesis of the NSD are discussed with special reference to its relation to glutamic acid.
en-copyright=
kn-copyright=

en-aut-name=NambaMasuyuki
en-aut-sei=Namba
en-aut-mei=Masuyuki
kn-aut-name=難波益之
kn-aut-sei=難波
kn-aut-mei=益之
aut-affil-num=1
ORCID=

en-aut-name=TanakaTakaho
en-aut-sei=Tanaka
en-aut-mei=Takaho
kn-aut-name=田中隆穂
kn-aut-sei=田中
kn-aut-mei=隆穂
aut-affil-num=2
ORCID=

en-aut-name=IshinoHirosi
en-aut-sei=Ishino
en-aut-mei=Hirosi
kn-aut-name=石野博志
kn-aut-sei=石野
kn-aut-mei=博志
aut-affil-num=3
ORCID=

en-aut-name=SenoHaruo
en-aut-sei=Seno
en-aut-mei=Haruo
kn-aut-name=妹尾晴夫
kn-aut-sei=妹尾
kn-aut-mei=晴夫
aut-affil-num=4
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=石津秀樹
kn-aut-sei=石津
kn-aut-mei=秀樹
aut-affil-num=5
ORCID=

en-aut-name=KurodaSigetosi
en-aut-sei=Kuroda
en-aut-mei=Sigetosi
kn-aut-name=黒田重利
kn-aut-sei=黒田
kn-aut-mei=重利
aut-affil-num=6
ORCID=

en-aut-name=KuyamaKeisuke
en-aut-sei=Kuyama
en-aut-mei=Keisuke
kn-aut-name=久山圭介
kn-aut-sei=久山
kn-aut-mei=圭介
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=慈圭精神医学研究所

affil-num=2
en-affil=
kn-affil=西宇部病院

affil-num=3
en-affil=
kn-affil=島根医科大学神経精神医学教室

affil-num=4
en-affil=
kn-affil=島根医科大学神経精神医学教室

affil-num=5
en-affil=
kn-affil=岡山大学医学部神経精神医学教室

affil-num=6
en-affil=
kn-affil=岡山大学医学部神経精神医学教室

affil-num=7
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=OPCA
kn-keyword=OPCA
en-keyword=Substantia nigra
kn-keyword=Substantia nigra
en-keyword=neuronal swelling degeneration
kn-keyword=neuronal swelling degeneration
en-keyword=glutamate
kn-keyword=glutamate
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=11-12
article-no=
start-page=1093
end-page=1105
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of guanidino compounds on monoamine oxidase and catechol-O-methyltransferase activity
kn-title=モノアミン代謝酵素活性に及ぼすグアニジノ化合物の影響に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the central nervous system (CNS)of mammals, monoamine oxidase (EC 1.4.3.4)(MAO), which have been divided into two functional forms (MAO-A and MAO-B), and catechol-O-methyltransferase (EC 2.1.1.6)(COMT) act as catabolic enzymes of catecholamines and serotonin regulating their concentrations. In this study, the effects of guanidino compounds (5mM) on MAO-A, MAO-B and COMT were examined to invastigate the role of guanidino compounds in CNS function. MAO-A activity was decreased by α-guanidinoglutaric acid (GGA) and guanidinoethanesulfonic acid, and increased by arginine (Arg) and N-acetylarginine at a low substrate concentration (4.33μM). MAO-B activity was decreased by creatinine (CRN), δ-guanidinovaleric acid (GVA) and methylguanidine (MGua) at a high substrate concentration (3.125mM), and decreased by CRN, GVA, MGua, Arg, guanidine, 2-guanidinoethanol, β-guanidinopropionic acid, guanidinosuccinic acid and homoarginine at a low substrate concentration (62.5μM). GVA, CRN and MGua acted as competitive inhibitors on MAO-B and their calculated Ki values were 9.47mM, 14.5mM and 29.4mM, respectively. Although the guanidino compounds tested had no effect on COMT activity at a high substrate concentration (600μM), GSA and GVA inhibited COMT activity at a low substrate concentration (75μM). These results suggest that some guanidino compounds influence catabolic enzymes of indoleamine and catecholamines to control CNS function.
en-copyright=
kn-copyright=

en-aut-name=HukuyamaKatsuhisa
en-aut-sei=Hukuyama
en-aut-mei=Katsuhisa
kn-aut-name=福山勝久
kn-aut-sei=福山
kn-aut-mei=勝久
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属分子細胞医学研究施設神経情報学部門
en-keyword=guanidino compounds
kn-keyword=guanidino compounds
en-keyword=monoamine oxidase A
kn-keyword=monoamine oxidase A
en-keyword=monoamine oxidase B
kn-keyword=monoamine oxidase B
en-keyword=chatechol-O-methyltransferase
kn-keyword=chatechol-O-methyltransferase
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=3-4
article-no=
start-page=221
end-page=234
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=1992
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of kainic acid, quisqualic acid and their antagonist on rat electrocorticoprams and on monoamine metabolite levels in rat striatum estimated by brain dialysis method
kn-title=カイニン酸, キスカル酸およびその拮抗薬投与にともなう脳波および線条体モノアミン代謝産物の変動
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The CNS action of kanie acid (KA), quisqualic acid (QA) and 1-(4-chlorobenzoyl)-piperazine-2, 3-dicarboxylic acid (pCB-PzDA) was investigated in male Sprague Dawley rats, and their effects on monoamina metabolite levels in rat striatum were studied using brain dialysis. Intracerebroventricularly injected KA and QA (100nmol) induced spike discharges, and pCB-PzDA (100nmol) suppressed electrocorticograms (ECoG) for 1 hour. pCB-PzDA aggravated KA induced spike discharges and inhibited QA-induced spike discharges. Dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels increased transitorily by injection of 100nmol and continuously by injection of 100nmol of KA. KA increased the 5-hydroxyindoleachtic acid (5-HIAA) level 2 hours after the administration dose-dependently. Though 10nmol of QA increased the HVA level slightly, 100nmol of QA increased the DOPAC, HVA and 5-HIAA levels. Though 100nmol of pCB-PzDA increased the DOPAC and HVA levels, it inhibited the increases in DOPAC, HVA and 5-HIAA levels induced by KA. On the other hand,pCB-PzDA inhibited the increases in DOPAC, HVA and 5-HIAA levels induced by QA for 1 hour, after which the DOPAC and HVA levels increased additively. These finding suggest that pCB-PzDA acts not only as a non-NMDA antagonist but also on dopaminergic neurons directly.
en-copyright=
kn-copyright=

en-aut-name=YamamotoMasatsune
en-aut-sei=Yamamoto
en-aut-mei=Masatsune
kn-aut-name=山本正恒
kn-aut-sei=山本
kn-aut-mei=正恒
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=kainic acid
kn-keyword=kainic acid
en-keyword=quisqualic acid
kn-keyword=quisqualic acid
en-keyword=pCB-PzDA
kn-keyword=pCB-PzDA
en-keyword=brain dialysis
kn-keyword=brain dialysis
en-keyword=monoamine metabolism
kn-keyword=monoamine metabolism
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=7-8
article-no=
start-page=769
end-page=778
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Striatal extracellular levels of dopamine and its metabolites during kainate-induced limbic seizures in freely-moving rats measured by brain microdialysis
kn-title=カイニン酸誘発けいれんにおける細胞外ドパミン量の経時的変化―脳内微小透析法を用いた実験的研究―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To investigate the role of brain dopaminergic systems in epilepsy, striatal extracellular levels of dopamins (DA) and its metabolites (3,4-dihydroxyphenylacetic acid : DOPAC and homovanillic acid : HVA) were measured during kainate-induced limbic seizures in freely-moving rats, using brain microdialysis. DA and its metabolites were measured by high performance liquid chromatography. Systemic injection of kainate (10mg/㎏, i. p.), which caused stable limbic seizures, significantly decreased the levels of DA and its metabolites. Intrahippocampal injection of kainae (2.5nmol), which also caused limbic seizures, significantly decreased only the DA levels, while DOPAC and HVA levels were unchanged. Similar to the results of the systemic injectjon, intrastriatal perfusion of kainate (10(-2) or 10(-6) M) significantly decreased the levels of DA, DOPAC and HVA in a dose-dependent manner. These findings indicate that, during kainate-induced limbic seizures, DA release was significantly reduced in the striatum. In conclusion, the hypofunction of striatal dopaminergic systems is related to the initiation and progress in epileptic seizures.
en-copyright=
kn-copyright=

en-aut-name=OhnishiMasaru
en-aut-sei=Ohnishi
en-aut-mei=Masaru
kn-aut-name=大西勝
kn-aut-sei=大西
kn-aut-mei=勝
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=kainate
kn-keyword=kainate
en-keyword=brain microdialysis
kn-keyword=brain microdialysis
en-keyword=dopamine
kn-keyword=dopamine
en-keyword=striatum
kn-keyword=striatum
en-keyword=epilepsy
kn-keyword=epilepsy
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=9-10
article-no=
start-page=1035
end-page=1051
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Experimental study of L-Dopa induced abnormal involuntary movements in monkey
kn-title=サルの L-Dopa 誘発不随意運動に関する実験的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hypokinesia in the unilateral limbs was induced in 8 monkeys (Macaca fuscata fuscata) by a lesion in the contralateral mesencepahlic ventromedial tegmentum (VMT). Daily oral administration of L-Dopa/carbidopa (40mg/kg, 4mg/kg) relieved the hypokinesia and thereafter induced continuous abnormal (choreo-athetoid) involuntary movements (AMI) in upper and lower limbs contralateral to the lesion. These movements were always uniform and continued for a few hours. The author performed a series of pharmacological studies using these VMT-lesioned monkeys. 1) Direct injection of dopamine (500-1000μg/10μl) and apomorphine (500-1500μg/10μl)into the dorsomedial part of the head of the caudate nucleus ipsilateral to the VMT lesion induced the same AIM as those induced by oral administration of L-Dopa/carbidopa. However, intraputaminal injection of these agents induced AIM in bucco-lingual region only. 2) After oral administration of L-Dopa/cabidopa, direct injection of methionine-enkephalin (300μg/10μl), GABA (500-1000μl/10μl) and serotonin (100-200μg/10μl) into the dorsomedial part of the head of the caudate nucleus (HCN) slightly decreased the AIM. However, substance p(200-400μg/10μl) or atropine (100-200μg/10μl) had no effect on the AIM. Neither the direct injection of GABA (500-1000μg/10μl) nor substance P (200-400μg/10μl) into the internal segment of the globus pallidus had any effect of the AIM. 3) The dopaminergic receptor (DA-2) binding study was performed on caudate tissues which were removed 5 weeks after creating the lesion in the unilateral VMT. DA-2 receptor binding of the dorsomedial part of the caudate nucleus, ipsilateral to the lesion, had a higher affinity than that of the ipsilateral ventrolateral part or the contralateral caudate tissue.
These results suggest that denervation supersensitivity of the post-synaptic DA-2 receptors in the dorsomedial part of the caudate nucleus is a basic condition for the development of L-Dopa induced AIM, and the postdopaninergic neuronal systems in the caudate nucleus are slightly suppressed by the intra-caudate neurons, of which transmitter substances are methionine-enkephalin, GABA and serotonin.
en-copyright=
kn-copyright=

en-aut-name=SakuraiMasaru
en-aut-sei=Sakurai
en-aut-mei=Masaru
kn-aut-name=桜井勝
kn-aut-sei=桜井
kn-aut-mei=勝
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳神経外科学教室
en-keyword=L-Dopa
kn-keyword=L-Dopa
en-keyword=involuntary movement
kn-keyword=involuntary movement
en-keyword=striatum
kn-keyword=striatum
en-keyword=centrally acting agents
kn-keyword=centrally acting agents
en-keyword=dopaminergic receptor
kn-keyword=dopaminergic receptor
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=9-10
article-no=
start-page=985
end-page=1002
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of δ-Guanidinovaleric acid and GABA agonists on monoamine release in rat striatum
kn-title=ラット脳線条体からのモノアミン放出におよぼす δ-Guanidinovaleric acid 及びGABA 受容体作動薬の影響に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=δ-Guanidinovaleric acid (GVA) is an endogenous convulsant and is thought to be a specific GABA antagonist. In the present study, we examined the effects of GVA and GABA agonists, GABA, muscimol and baclofen, on dopamine and serotonin releases in rat striatum using a brain dialysis technique. GVA produced a significant increase in DA released transiently (1mM) and throughout the experiment (10mM) compared with the controls. It also produced a significant increase in 5-HT release in both concentrations throughout the experiment. GABA (10mM) inhibited DA and 5-HT releases induced by GVA. Muscimol (10mM) inhibited DA and 5-HT releases induced by GVA. Especially muscimol was more effective in the inhibition of 5-HT release. Baclofen (10mM) inhibited only DA release induced by GVA. These results suggest that the activation of GABA receptor inhibits the release of DA and 5-HT in the striatum, and that the DAergic system regulates the GABA-B receptor while the 5-HTergic system mainly regulates the GABA-A receptor.
en-copyright=
kn-copyright=

en-aut-name=IwayaKazuo
en-aut-sei=Iwaya
en-aut-mei=Kazuo
kn-aut-name=岩谷和夫
kn-aut-sei=岩谷
kn-aut-mei=和夫
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属分子細胞医学研究施設神経情報学部門
en-keyword=δ-Guanidinovaleric acid
kn-keyword=δ-Guanidinovaleric acid
en-keyword=GABA(A) receptor
kn-keyword=GABA(A) receptor
en-keyword=GABA(B) receptor
kn-keyword=GABA(B) receptor
en-keyword=Serotonin
kn-keyword=Serotonin
en-keyword=Dopamine
kn-keyword=Dopamine
END

start-ver=1.4
cd-journal=joma
no-vol=107
cd-vols=
no-issue=7-8
article-no=
start-page=131
end-page=141
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=19950831
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Adenosines as preventive preparations of post-traumatic epilepsy
kn-title=アデノシン関連物質による外傷性てんかん発症予防に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=As oxidation of neural membranes by reactive oxygen species (ROS), especially hydroxyl radicals (・OH), is involved in the biochemical pathogenesis of post-traumatic epilepsy, post-traumatic epilepsy is thought to be prevented by treatment with ROS scavengers. In the present study, I first examined the effects of adenosine (Ado), 2-chloroadenosine (CI-Ado) and guanosine on ・OH and superoxide anion (O(-)(2)), generated by the Fenton reagent and the hypoxanthine-xanthine oxidase system, respectively, using electron spin resonance spectrometry. I also examined the effecta of Ado and Cl-Ado on the occurrence of epileptic discharges on the electrocorticogram (ECoG) induced by FeCl(3) injection (500nmol) into the sensorimotor cortex of rats, i.e., a model of an experimental post-traumatic epilepsy. Although O(-)(2) was not scavenged, ・OH were scavenged by Ado and Cl-Ado dose-dependently. The scavenging activity of Ado was 4 times stronger then thst of Cl-Ado. On the ECoG of rats given FeCl(3), sporadic spike discharges, polyspikes and/or ictal patterns started to be observed 15-90 min after the injection. Epileptic discharges did not appear or their occurrence was delayed by the intraperitioneal injection of Ado (5mg/kg) or Cl-Ado (1mg/kg) 30 min prior to the FeCl(3) injection, although Cl-Ado showed a chronotropic action. Thus Ado and Ci-Ado may be useful in the prevention and the attenuation of progression of post-traumatic epilepsy by scavenging ・OH and by their anticonvulsant effect.
en-copyright=
kn-copyright=

en-aut-name=TomaJunji
en-aut-sei=Toma
en-aut-mei=Junji
kn-aut-name=当真純二
kn-aut-sei=当真
kn-aut-mei=純二
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属分子細胞医学研究施設神経情報学部門
en-keyword=adenosine
kn-keyword=adenosine
en-keyword=chloroadenosine
kn-keyword=chloroadenosine
en-keyword=radical scavenger
kn-keyword=radical scavenger
en-keyword=post-traumatic epilepsy
kn-keyword=post-traumatic epilepsy
en-keyword=experimental epilepsy
kn-keyword=experimental epilepsy
END

start-ver=1.4
cd-journal=joma
no-vol=116
cd-vols=
no-issue=1
article-no=
start-page=17
end-page=27
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20040531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Parkinson's disease from a viewpoint of regenerative medicine
kn-title=再生医学から見たパーキンソン病
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It has long been considered that central nervous system would not regenerate after injury, but this concept has recently been changing due to the development of neuroscience research. Cell grafting, gene transfer and neurotrophic factor administration into the brain and spinal cord are the examples of methods to perform protection and repair. These techniques are expected to be applied to certain neurological disorders such as Parkinson's disease, cerebral ischemia and spinal cord injury. Parkinson's disease is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the nigrostriatal system. Fetal neurons, chromaffin cells, cell lines, certain genes, neural stem cells, ES cells and bone marrow cells have been investigated as donor cells and vectors to treat Parkinson's disease. This review will summarize the history of neural transplantation in Parkinson's disease and features and prospects of each donor will be discussed.
en-copyright=
kn-copyright=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=伊達勲
kn-aut-sei=伊達
kn-aut-mei=勲
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯学総合研究科　神経病態外科学
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
en-keyword=neural transplantation
kn-keyword=neural transplantation
en-keyword=regeneration
kn-keyword=regeneration
END

start-ver=1.4
cd-journal=joma
no-vol=118
cd-vols=
no-issue=2
article-no=
start-page=99
end-page=103
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060901
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=中枢神経疾患に対するカプセル化細胞移植
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=安原隆雄
kn-aut-sei=安原
kn-aut-mei=隆雄
aut-affil-num=1
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=新郷哲郎
kn-aut-sei=新郷
kn-aut-mei=哲郎
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=小林和樹
kn-aut-sei=小林
kn-aut-mei=和樹
aut-affil-num=3
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=竹内亮
kn-aut-sei=竹内
kn-aut-mei=亮
aut-affil-num=4
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=矢野昭正
kn-aut-sei=矢野
kn-aut-mei=昭正
aut-affil-num=5
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=村岡賢一郎
kn-aut-sei=村岡
kn-aut-mei=賢一郎
aut-affil-num=6
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=亀田雅博
kn-aut-sei=亀田
kn-aut-mei=雅博
aut-affil-num=7
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=元文姫
kn-aut-sei=元
kn-aut-mei=文姫
aut-affil-num=8
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=早瀬仁志
kn-aut-sei=早瀬
kn-aut-mei=仁志
aut-affil-num=9
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=上利崇
kn-aut-sei=上利
kn-aut-mei=崇
aut-affil-num=10
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=松井利浩
kn-aut-sei=松井
kn-aut-mei=利浩
aut-affil-num=11
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=三好康之
kn-aut-sei=三好
kn-aut-mei=康之
aut-affil-num=12
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=伊達勲
kn-aut-sei=伊達
kn-aut-mei=勲
aut-affil-num=13
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=11
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=12
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科

affil-num=13
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科
en-keyword=カプセル化細胞移植
kn-keyword=カプセル化細胞移植
en-keyword=グリア細胞株由来神経栄養因子 (GDNF)
kn-keyword=グリア細胞株由来神経栄養因子 (GDNF)
en-keyword=血管内皮成長因子 (VEGF)
kn-keyword=血管内皮成長因子 (VEGF)
en-keyword=脳虚血
kn-keyword=脳虚血
en-keyword=パーキンソン病
kn-keyword=パーキンソン病
END

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=3
article-no=
start-page=235
end-page=239
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Quinone formation as a common neurotoxic factor in dopaminergic neurotoxicity induced by an excess amount of cytosolic dopamine
kn-title=小胞外過剰ドパミンによるドパミン神経障害における共通因子としてのキノン体生成
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=宮崎育子
kn-aut-sei=宮崎
kn-aut-mei=育子
aut-affil-num=1
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=浅沼幹人
kn-aut-sei=浅沼
kn-aut-mei=幹人
aut-affil-num=2
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=Francisco J.Diaz-Corrales
kn-aut-sei=Francisco J.
kn-aut-mei=Diaz-Corrales
aut-affil-num=3
ORCID=

en-aut-name=MiyoshiKo
en-aut-sei=Miyoshi
en-aut-mei=Ko
kn-aut-name=三好耕
kn-aut-sei=三好
kn-aut-mei=耕
aut-affil-num=4
ORCID=

en-aut-name=OgawaNorio
en-aut-sei=Ogawa
en-aut-mei=Norio
kn-aut-name=小川紀雄
kn-aut-sei=小川
kn-aut-mei=紀雄
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科 神経情報学
en-keyword=ドパミンキノン
kn-keyword=ドパミンキノン
en-keyword=パーキンソン病
kn-keyword=パーキンソン病
en-keyword=メタンフェタミン
kn-keyword=メタンフェタミン
en-keyword=キノン還元酵素
kn-keyword=キノン還元酵素
en-keyword=チロシナーゼ
kn-keyword=チロシナーゼ
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=虚血後線状体に出現する神経前駆細胞の起源
kn-title=Subventricular Zone-Derived Neuroblasts Migrate and Differentiate into Mature Neurons in the Post-Stroke Adult Striatum
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent studies have revealed that the adult mammalian brain has the capacity to regenerate some neurons after various insults. However, the precise mechanism of insult-induced neurogenesis has not been demonstrated. In the normal brain, GFAP-expressing cells in the subventricular zone (SVZ) of the lateral ventricles include a neurogenic cell population that gives rise to olfactory bulb neurons only. Herein, we report evidence that, after a stroke, these cells are capable of producing new neurons outside the olfactory bulbs. SVZ GFAP-expressing cells labeled by a cell-type-specific viral infection method were found to generate neuroblasts that migrated toward the injured striatum after middle cerebral artery occlusion. These neuroblasts in the striatum formed elongated chain-like cell aggregates similar to those in the normal SVZ, and these chains were observed to be closely associated with thin astrocytic processes and blood vessels. Finally, long-term tracing of the green fluorescent-labeled cells with a Cre-loxP system revealed that the SVZ-derived neuroblasts differentiated into mature neurons in the striatum, in which they expressed neuronal-specific nuclear protein and formed synapses with neighboring striatal cells. These results highlight the role of the SVZ in neuronal regeneration after a stroke and its potential as an important therapeutic target for various neurological disorders.
en-copyright=
kn-copyright=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=山下徹
kn-aut-sei=山下
kn-aut-mei=徹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
en-keyword=zone
kn-keyword=zone
en-keyword=cerebral ischemia
kn-keyword=cerebral ischemia
en-keyword=migration
kn-keyword=migration
en-keyword=neurogenesis
kn-keyword=neurogenesis
en-keyword=regeneration
kn-keyword=regeneration
en-keyword=striatum
kn-keyword=striatum
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ラット線条体内Golf蛋白量は抗うつ薬慢性投与により増加し嗅球摘出術により減少する
kn-title=Golf protein levels in rat striatum are increased by chronic antidepressant administration and decreased by olfactory bulbectomy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TaokaHideki
en-aut-sei=Taoka
en-aut-mei=Hideki
kn-aut-name=田岡秀樹
kn-aut-sei=田岡
kn-aut-mei=秀樹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=メタンフェタミン誘発ドパミン神経毒性はキノン体形成関連分子により調節されている
kn-title=Methamphetamine-induced dopaminergic neurotoxicity is regulated by quinone formation-related molecules
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recently, the neurotoxicity of dopamine (DA) quinone formation by auto-oxidation of DA has focused on dopaminergic neuron-specific oxidative stress. In the present study, we examined DA quinone formation in methamphetamine (METH)-induced dopaminergic neuronal cell death using METH-treated dopaminergic cultured CATH.a cells and METH-injected mouse brain. In CATH.a cells, METH treatment dose-dependently increased the levels of quinoprotein (protein-bound quinone) and the expression of quinone reductase in parallel with neurotoxicity. A similar increase in quinoprotein levels was seen in the striatum of METH (4 mg/kg X4, i.p., 2 h interval)-injected BALB/c mice, coinciding with reduction of DA transporters. Furthermore, pretreatment of CATH.a cells with quinone reductase inducer, butylated hydroxyanisole, significantly and dose-dependently blocked METH-induced elevation of quinoprotein, and ameliorated METH-induced cell death. We also showed the protective effect of tyrosinase, which rapidly oxidizes DA and DA quinone to form stable melanin, against METH-induced dopaminergic neurotoxicity in vitro and in vivo using tyrosinase null mice. Our results indicate that DA quinone formation plays an important role, as a dopaminergic neuron-specific neurotoxic factor, in METH-induced neurotoxicity, which is regulated by quinone formation-related molecules.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=宮﨑育子
kn-aut-sei=宮﨑
kn-aut-mei=育子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
en-keyword=dopamine quinone
kn-keyword=dopamine quinone
en-keyword=quinone reductase
kn-keyword=quinone reductase
en-keyword=tyrosinase
kn-keyword=tyrosinase
END

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