start-ver=1.4
cd-journal=joma
no-vol=165
cd-vols=
no-issue=
article-no=
start-page=106013
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202409
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Salivary buffering capacity is correlated with umami but not sour taste sensitivity in healthy adult Japanese subjects
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: Saliva serves multiple important functions crucial for maintaining a healthy oral and systemic environment. Among them, the pH buffering effect, which is primarily mediated by bicarbonate ions, helps maintain oral homeostasis by neutralizing acidity from ingested foods. Therefore, higher buffering capacity, reflecting the ability to neutralize oral acidity, may influence taste sensitivity, especially for sour taste since it involves sensing H+ ions. This study aims to explore the relationship between salivary buffering capacity and taste sensitivities to the five basic tastes in healthy adult humans.
Design: Eighty seven healthy adult students participated in this study. Resting saliva volume was measured using the spitting method. The liquid colorimetric test was used to assess salivary buffering capacity. The whole-mouth taste testing method was employed to determine the recognition threshold for each tastant (NaCl, sucrose, citric acid, quinine-HCl, monosodium glutamate).
Results: Taste recognition thresholds for sour taste as well as sweet, salty, and bitter tastes showed no correlation with salivary buffering capacity. Interestingly, a negative relationship was observed between recognition threshold for umami taste and salivary buffering capacity. Furthermore, a positive correlation between salivary buffering capacity and resting saliva volume was observed.
Conclusions: Salivary buffering capacity primarily influences sensitivity to umami taste, but not sour and other tastes.
en-copyright=
kn-copyright=
en-aut-name=HyodoAiko
en-aut-sei=Hyodo
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MikamiAyaka
en-aut-sei=Mikami
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=IidaSeiji
en-aut-sei=Iida
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=4
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=5
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=6
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=7
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=taste recognition threshold
kn-keyword=taste recognition threshold
en-keyword=resting saliva
kn-keyword=resting saliva
en-keyword=bicarbonate
kn-keyword=bicarbonate
en-keyword=xerostomia
kn-keyword=xerostomia
en-keyword=TAS1R
kn-keyword=TAS1R
END
start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=16
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Sugar signals from oral glucose transporters elicit cephalic-phase insulin release in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cephalic-phase insulin release (CPIR) occurs before blood glucose increases after a meal. Although glucose is the most plausible cue to induce CPIR, peripheral sensory systems involved are not fully elucidated. We therefore examined roles of sweet sensing by a T1R3-dependent taste receptor and sugar sensing by oral glucose transporters in the oropharyngeal region in inducing CPIR. Spontaneous oral ingestion of glucose significantly increased plasma insulin 5 min later in wild-type (C57BL/6) and T1R3-knockout mice, but intragastric infusion did not. Oral treatment of glucose transporter inhibitors phlorizin and phloretin significantly reduced CPIR after spontaneous oral ingestion. In addition, a rapid increase in plasma insulin was significantly smaller in WT mice with spontaneous oral ingestion of nonmetabolizable glucose analog than in WT mice with spontaneous oral ingestion of glucose. Taken together, the T1R3-dependent receptor is not required for CPIR, but oral glucose transporters greatly contribute to induction of CPIR by sugars.
en-copyright=
kn-copyright=
en-aut-name=TakamoriMitsuhito
en-aut-sei=Takamori
en-aut-mei=Mitsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=EgusaMasahiko
en-aut-sei=Egusa
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MiyawakiTakuya
en-aut-sei=Miyawaki
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=4
en-affil=The Center for Special Needs Dentistry, Okayama University Hospital
kn-affil=
affil-num=5
en-affil=Department of Dental Anesthesiology and Special Care Dentistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Cephalic-phase insulin response
kn-keyword=Cephalic-phase insulin response
en-keyword=Glucose transporters
kn-keyword=Glucose transporters
en-keyword=Glucose
kn-keyword=Glucose
en-keyword=Sweet taste receptor
kn-keyword=Sweet taste receptor
en-keyword=Food intake
kn-keyword=Food intake
END
start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=13
article-no=
start-page=2941
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230628
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Adrenomedullin Enhances Mouse Gustatory Nerve Responses to Sugars via T1R-Independent Sweet Taste Pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=On the tongue, the T1R-independent pathway (comprising glucose transporters, including sodium-glucose cotransporter (SGLT1) and the K-ATP channel) detects only sugars, whereas the T1R-dependent (T1R2/T1R3) pathway can broadly sense various sweeteners. Cephalic-phase insulin release, a rapid release of insulin induced by sensory signals in the head after food-related stimuli, reportedly depends on the T1R-independent pathway, and the competitive sweet taste modulators leptin and endocannabinoids may function on these two different sweet taste pathways independently, suggesting independent roles of two oral sugar-detecting pathways in food intake. Here, we examined the effect of adrenomedullin (ADM), a multifunctional regulatory peptide, on sugar sensing in mice since it affects the expression of SGLT1 in rat enterocytes. We found that ADM receptor components were expressed in T1R3-positive taste cells. Analyses of chorda tympani (CT) nerve responses revealed that ADM enhanced responses to sugars but not to artificial sweeteners and other tastants. Moreover, ADM increased the apical uptake of a fluorescent D-glucose derivative into taste cells and SGLT1 mRNA expression in taste buds. These results suggest that the T1R-independent sweet taste pathway in mouse taste cells is a peripheral target of ADM, and the specific enhancement of gustatory nerve responses to sugars by ADM may contribute to caloric sensing and food intake.
en-copyright=
kn-copyright=
en-aut-name=IwataShusuke
en-aut-sei=Iwata
en-aut-mei=Shusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TakaiShingo
en-aut-sei=Takai
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=SanematsuKeisuke
en-aut-sei=Sanematsu
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=ShigemuraNoriatsu
en-aut-sei=Shigemura
en-aut-mei=Noriatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=3
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=4
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=5
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=taste
kn-keyword=taste
en-keyword=sweet taste
kn-keyword=sweet taste
en-keyword=taste receptor family 1 members 2 and 3
kn-keyword=taste receptor family 1 members 2 and 3
en-keyword=sodium-glucose cotransporter 1
kn-keyword=sodium-glucose cotransporter 1
en-keyword=adrenomedullin
kn-keyword=adrenomedullin
en-keyword=caloric sensing
kn-keyword=caloric sensing
END
start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=6
article-no=
start-page=1150
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Taste Responses and Ingestive Behaviors to Ingredients of Fermented Milk in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Fermented milk is consumed worldwide because of its nutritious and healthful qualities. Although it is somewhat sour, causing some to dislike it, few studies have examined taste aspects of its ingredients. Wild-type mice and T1R3-GFP-KO mice lacking sweet/umami receptors were tested with various taste components (sucrose, galactose, lactose, galacto-oligosaccharides, fructo-oligosaccharides, l- and d-lactic acid) using 48 h two-bottle tests and short-term lick tests. d-lactic acid levels were measured after the ingestion of d- or; l-lactic acid or water to evaluate d-lactic acidosis. In wild-type mice, for the sweet ingredients the number of licks increased in a concentration-dependent manner, but avoidance was observed at higher concentrations in 48 h two-bottle tests; the sour ingredients d- and l-lactic acid showed concentration-dependent decreases in preference in both short- and long-term tests. In 48 h two-bottle tests comparing d- and l-lactic acid, wild-type but not T1R3-GFP-KO mice showed higher drinking rates for l-lactic acid. d-lactic acidosis did not occur and thus did not contribute to this preference. These results suggest that intake in short-term lick tests varied by preference for each ingredient, whereas intake variation in long-term lick tests reflects postingestive effects. l-lactic acid may have some palatable taste in addition to sour taste.
en-copyright=
kn-copyright=
en-aut-name=YamaseYuko
en-aut-sei=Yamase
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=HuangHai
en-aut-sei=Huang
en-aut-mei=Hai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=EgusaMasahiko
en-aut-sei=Egusa
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=MiyawakiTakuya
en-aut-sei=Miyawaki
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Department of Dental Anesthesiology and Special Care Dentistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=4
en-affil=Department of Dental Anesthesiology and Special Care Dentistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=5
en-affil=Department of Dental Anesthesiology and Special Care Dentistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=postingestive effects
kn-keyword=postingestive effects
en-keyword=galactose
kn-keyword=galactose
en-keyword=lactose
kn-keyword=lactose
en-keyword=oligosaccharides
kn-keyword=oligosaccharides
en-keyword=lactic acid
kn-keyword=lactic acid
END
start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=
article-no=
start-page=57
end-page=63
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The sweet taste receptor, glucose transporters, and the ATP-sensitive K+ (KATP) channel: sugar sensing for the regulation of energy homeostasis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sugar detection in the oral cavity does not solely depend on the TAS1R2 + TAS1R3 sweet receptor. Similar to gut, pancreas, and hypothalamic neurons, in the tongue glucose transporters and ATP-sensitive K+ (KATP) channels are also involved in sugar detection. Among them, the KATP channel is the target for the antiobesity hormone leptin, which inhibits sugar-sensitive cells such as sweet taste cells, pancreatic β-cells, and hypothalamic orexigenic neurons. Sugar signals from the taste organ elicit cephalic-phase insulin release, and those from the gut contribute to sweet preference for caloric sugars. All of these systems are indispensable for maintaining energy homeostasis. Thus, an exquisite system for sugar detection/signaling to regulate energy homeostasis exists in our body.
en-copyright=
kn-copyright=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=YasumatsuKeiko
en-aut-sei=Yasumatsu
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=2
en-affil=Tokyo Dental Junior College
kn-affil=
affil-num=3
en-affil=Division of Sensory Physiology and Medical Application Sensing, Research and Development Center for Five-Sense Devices, Kyushu University
kn-affil=
en-keyword=gustatory nerve fibers
kn-keyword=gustatory nerve fibers
en-keyword=leptin
kn-keyword=leptin
en-keyword=cephalic-phase insulin release
kn-keyword=cephalic-phase insulin release
en-keyword=sweet taste
kn-keyword=sweet taste
en-keyword=food intake
kn-keyword=food intake
END
start-ver=1.4
cd-journal=joma
no-vol=158
cd-vols=
no-issue=
article-no=
start-page=233
end-page=245
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phosphatidylinositol‐3 kinase mediates the sweet suppressive effect of leptin in mouse taste cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Leptin is known to selectively suppress neural and taste cell responses to sweet compounds. The sweet suppressive effect of leptin is mediated by the leptin receptor Ob‐Rb, and the ATP‐gated K+ (KATP) channel expressed in some sweet‐sensitive, taste receptor family 1 member 3 (T1R3)‐positive taste cells. However, the intracellular transduction pathway connecting Ob‐Rb to KATP channel remains unknown. Here we report that phosphoinositide 3‐kinase (PI3K) mediates leptin's suppression of sweet responses in T1R3‐positive taste cells. In in situ taste cell recording, systemically administrated leptin suppressed taste cell responses to sucrose in T1R3‐positive taste cells. Such leptin's suppression of sucrose responses was impaired by co‐administration of PI3K inhibitors (wortmannin or LY294002). In contrast, co‐administration of signal transducer and activator of transcription 3 inhibitor (Stattic) or Src homology region 2 domain‐containing phosphatase‐2 inhibitor (SHP099) had no effect on leptin's suppression of sucrose responses, although signal transducer and activator of transcription 3 and Src homology region 2 domain‐containing phosphatase‐2 were expressed in T1R3‐positive taste cells. In peeled tongue epithelium, phosphatidylinositol (3,4,5)‐trisphosphate production and phosphorylation of AKT by leptin were immunohistochemically detected in some T1R3‐positive taste cells but not in glutamate decarboxylase 67‐positive taste cells. Leptin‐induced phosphatidylinositol (3,4,5)‐trisphosphate production was suppressed by LY294002. Thus, leptin suppresses sweet responses of T1R3‐positive taste cells by activation of Ob‐Rb–PI3K–KATP channel pathway.
en-copyright=
kn-copyright=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MargolskeeRobert F.
en-aut-sei=Margolskee
en-aut-mei=Robert F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=2
en-affil=Monell Chemical Senses Center
kn-affil=
affil-num=3
en-affil=Monell Chemical Senses Center
kn-affil=
en-keyword=energy homeostasis
kn-keyword=energy homeostasis
en-keyword=leptin signaling
kn-keyword=leptin signaling
en-keyword=metabolic sensor
kn-keyword=metabolic sensor
en-keyword=obesity
kn-keyword=obesity
en-keyword=sweet receptor cell
kn-keyword=sweet receptor cell
END
start-ver=1.4
cd-journal=joma
no-vol=228
cd-vols=
no-issue=
article-no=
start-page=102712
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202011
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Orexin A and B in the rat superior salivatory nucleus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Orexin (OX), which regulates sleep and wakefulness and feeding behaviors has 2 isoforms, orexin-A and -B (OXA and OXB). In this study, the distribution of OXA and OXB was examined in the rat superior salivatory nucleus (SSN) using retrograde tracing and immunohistochemical and methods. OXA- and OXB-immunoreactive (-ir) nerve fibers were seen throughout the SSN. These nerve fibers surrounded SSN neurons retrogradely labeled with Fast blue (FB) from the corda-lingual nerve. FB-positive neurons had pericellular OXA- (47.5%) and OXB-ir (49.0%) nerve fibers. Immunohistochemistry for OX receptors also demonstrated the presence of OX1R and OX2R in FB-positive SSN neurons. The majority of FB-positive SSN neurons contained OX1R- (69.7%) or OX2R-immunoreactivity (57.8%). These neurons had small and medium-sized cell bodies. In addition, half of FB-positive SSN neurons which were immunoreactive for OX1R (47.0%) and OX2R (52.2%) had pericellular OXA- and OXB-ir nerve fibers, respectively. Co-expression of OX1R- and OX2R was common in FB-positive SSN neurons. The present study suggests a possibility that OXs regulate the activity of SSN neurons through OX receptors.
en-copyright=
kn-copyright=
en-aut-name=SatoTadasu
en-aut-sei=Sato
en-aut-mei=Tadasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=YajimaTakehiro
en-aut-sei=Yajima
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=FujitaMasako
en-aut-sei=Fujita
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=KobashiMotoi
en-aut-sei=Kobashi
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=IchikawaHiroyuki
en-aut-sei=Ichikawa
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
affil-num=1
en-affil=Division of Oral and Craniofacial Anatomy, Tohoku University Graduate School of Dentistry
kn-affil=
affil-num=2
en-affil=Division of Oral and Craniofacial Anatomy, Tohoku University Graduate School of Dentistry
kn-affil=
affil-num=3
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Division of Oral and Craniofacial Anatomy, Tohoku University Graduate School of Dentistry
kn-affil=
affil-num=6
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine and Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Orexin
kn-keyword=Orexin
en-keyword=Orexin receptor
kn-keyword=Orexin receptor
en-keyword=Superior salivatory nucleus
kn-keyword=Superior salivatory nucleus
en-keyword=Preganglionic neuron
kn-keyword=Preganglionic neuron
en-keyword=Chorda-lingual nerve
kn-keyword=Chorda-lingual nerve
en-keyword=Immunohistochemistry
kn-keyword=Immunohistochemistry
END
start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=12
article-no=
start-page=4422
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200622
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Effects of Mutual Interaction of Orexin-A and Glucagon-Like Peptide-1 on Reflex Swallowing Induced by SLN Afferents in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=(1) Background: Our previous studies revealed that orexin-A, an appetite-increasing peptide, suppressed reflex swallowing via the commissural part of the nucleus tractus solitarius (cNTS), and that glucagon-like peptide-1 (GLP-1), an appetite-reducing peptide, also suppressed reflex swallowing via the medial nucleus of the NTS (mNTS). In this study, we examined the mutual interaction between orexin-A and GLP-1 in reflex swallowing. (2) Methods: Sprague-Dawley rats under urethane-chloralose anesthesia were used. Swallowing was induced by electrical stimulation of the superior laryngeal nerve (SLN) and was identified by the electromyographic (EMG) signals obtained from the mylohyoid muscle. (3) Results: The injection of GLP-1 (20 pmol) into the mNTS reduced the swallowing frequency and extended the latency of the first swallow. These suppressive effects of GLP-1 were not observed after the fourth ventricular administration of orexin-A. After the injection of an orexin-1 receptor antagonist (SB334867) into the cNTS, an ineffective dose of GLP-1 (6 pmol) into the mNTS suppressed reflex swallowing. Similarly, the suppressive effects of orexin-A (1 nmol) were not observed after the injection of GLP-1 (6 pmol) into the mNTS. After the administration of a GLP-1 receptor antagonist (exendin-4(5-39)), an ineffective dose of orexin-A (0.3 nmol) suppressed reflex swallowing. (4) Conclusions: The presence of reciprocal inhibitory connections between GLP-1 receptive neurons and orexin-A receptive neurons in the NTS was strongly suggested.
en-copyright=
kn-copyright=
en-aut-name=KobashiMotoi
en-aut-sei=Kobashi
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=ShimataniYuichi
en-aut-sei=Shimatani
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=FujitaMasako
en-aut-sei=Fujita
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=MatsuoRyuji
en-aut-sei=Matsuo
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Medical Engineering, Faculty of Science and Engineering, Tokyo City University
kn-affil=
affil-num=3
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=GLP-1
kn-keyword=GLP-1
en-keyword=orexin
kn-keyword=orexin
en-keyword=SB334867
kn-keyword=SB334867
en-keyword=swallowing
kn-keyword=swallowing
en-keyword=NTS
kn-keyword=NTS
en-keyword=rats
kn-keyword=rats
END
start-ver=1.4
cd-journal=joma
no-vol=369
cd-vols=
no-issue=
article-no=
start-page=29
end-page=39
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180115
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bitter Taste Responses of Gustducin-positive Taste Cells in Mouse Fungiform and Circumvallate Papillae
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Bitter taste serves as an important signal for potentially poisonous compounds in foods to avoid their ingestion. Thousands of compounds are estimated to taste bitter and presumed to activate taste receptor cells expressing bitter taste receptors (Tas2rs) and coupled transduction components including gustducin, phospholipase Cβ2 (PLCβ2) and transient receptor potential channel M5 (TRPM5). Indeed, some gustducin-positive taste cells have been shown to respond to bitter compounds. However, there has been no systematic characterization of their response properties to multiple bitter compounds and the role of transduction molecules in these cells. In this study, we investigated bitter taste responses of gustducin-positive taste cells in situ in mouse fungiform (anterior tongue) and circumvallate (posterior tongue) papillae using transgenic mice expressing green fluorescent protein in gustducin-positive cells. The overall response profile of gustducin-positive taste cells to multiple bitter compounds (quinine, denatonium, cyclohexamide, caffeine, sucrose octaacetate, tetraethylammonium, phenylthiourea, L-phenylalanine, MgSO4, and high concentration of saccharin) was not significantly different between fungiform and circumvallate papillae. These bitter-sensitive taste cells were classified into several groups according to their responsiveness to multiple bitter compounds. Bitter responses of gustducin-positive taste cells were significantly suppressed by inhibitors of TRPM5 or PLCβ2. In contrast, several bitter inhibitors did not show any effect on bitter responses of taste cells. These results indicate that bitter-sensitive taste cells display heterogeneous responses and that TRPM5 and PLCβ2 are indispensable for eliciting bitter taste responses of gustducin-positive taste cells.
en-copyright=
kn-copyright=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TakaiShingo
en-aut-sei=Takai
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SanematsuKeisuke
en-aut-sei=Sanematsu
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MargolskeeRobert F.
en-aut-sei=Margolskee
en-aut-mei=Robert F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=ShigemuraNoriatsu
en-aut-sei=Shigemura
en-aut-mei=Noriatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=2
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=3
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=4
en-affil=Monell Chemical Senses Center
kn-affil=
affil-num=5
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
affil-num=6
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=
en-keyword=bitter antagonists
kn-keyword=bitter antagonists
en-keyword=bitter receptor
kn-keyword=bitter receptor
en-keyword=breadth of responsiveness
kn-keyword=breadth of responsiveness
en-keyword=taste coding
kn-keyword=taste coding
en-keyword=transgenic mouse
kn-keyword=transgenic mouse
END
start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=135041
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200513
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of Bitter Receptor Antagonists on Behavioral Lick Responses of Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Bitter taste receptors TAS2Rs detect noxious compounds in the oral cavity. Recent heterologous expression studies reported that some compounds function as antagonists for human TAS2Rs. For examples, amino acid derivatives such as γ-aminobutyric acid (GABA) and Nα,Nα-bis(carboxymethyl)-L-Lysine (BCML) blocked responses to quinine mediated by human TAS2R4. Probenecid inhibited responses to phenylthiocarbamide mediated by human TAS2R38. In this study, we investigated the effects of these human bitter receptor antagonists on behavioral lick responses of mice to elucidate whether these compounds also function as bitter taste blockers. In short-term (10 s) lick tests, concentration-dependent lick responses to bitter compounds (quinine-HCl, denatonium and phenylthiourea) were not affected by the addition of GABA or BCML. Probenecid reduced aversive lick responses to denatonium and phenylthiourea but not to quinine-HCl. In addition, taste cell responses to phenylthiourea were inhibited by probenecid. These results suggest some bitter antagonists of human TAS2Rs can work for bitter sense of mouse.
en-copyright=
kn-copyright=
en-aut-name=MasamotoMichimasa
en-aut-sei=Masamoto
en-aut-mei=Michimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KobashiMotoi
en-aut-sei=Kobashi
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=ShigemuraNoriatsu
en-aut-sei=Shigemura
en-aut-mei=Noriatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
affil-num=4
en-affil=Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University
kn-affil=
affil-num=5
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=bitter coding
kn-keyword=bitter coding
en-keyword=bitter inhibitor
kn-keyword=bitter inhibitor
en-keyword=gustatory response
kn-keyword=gustatory response
en-keyword=species difference
kn-keyword=species difference
en-keyword=taste perception
kn-keyword=taste perception
END