JaLCDOI 10.18926/AMO/48264
FullText URL 66_2_143.pdf.pdf
Author Watanabe, Makiko| Ueno, Hiroshi| Suemitsu, Shunsuke| Yokobayashi, Eriko| Matsumoto, Yosuke| Usui, Shinichi| Sujiura, Hiroko| Okamoto, Motoi|
Abstract Recent studies have demonstrated the important role of immune molecules in the development of neuronal circuitry and synaptic plasticity. We have detected the presence of FcγRllB protein in parvalbumin- containing inhibitory interneurons (PV neurons). In the present study, we examined the appearance of PV neurons in the barrel cortex and the effect of sensory deprivation in FcγRllB-deficient mice (FcγRllB-/-) and wild-type mice. There was no substantial difference in the appearance of PV neurons in the developing barrel cortex between FcγRllB-/- and wild-type mice. Sensory deprivation from immediately after birth (P0) or P7 to P12-P14 induced an increase in PV neurons. In contrast, sensory deprivation from P7 or P14 to P28, but not from P21 to P28, decreased PV neurons in wild-type mice. However, sensory deprivation from P0 or P7 to P12-P14 did not increase PV neurons and sensory deprivation from P7 or P14 to P28 did not decrease or only modestly decreased PV neurons in FcγRllB-/- mice. The results indicate that expression of PV is regulated by sensory experience and the second and third postnatal weeks are a sensitive period for sensory deprivation, and suggest that FcγRllB contributes to sensory experience-regulated expression of PV.
Keywords parvalbumin fast-spiking interneurons FcγRllB barrel cortex sensory deprivation
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-04
Volume volume66
Issue issue2
Publisher Okayama University Medical School
Start Page 143
End Page 154
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22525472
Web of Science KeyUT 000303175300007
JaLCDOI 10.18926/AMO/50406
FullText URL 67_3_135.pdf
Author Ueno, Hiroshi| Shoshi, Chikafumi| Suemitsu, Shunsuke| Usui, Shinichi| Sujiura, Hiroko| Okamoto, Motoi|
Abstract In the phenomenon known as cross-modal plasticity, the loss of one sensory system is followed by improved functioning of other intact sensory systems. MRI and functional MRI studies suggested a role of the prefrontal cortex and the temporal lobe in cross-modal plasticity. We used a mouse model to examine the effects of sensory deprivation achieved by whisker trimming and visual deprivation achieved by dark rearing in neonatal mice on the appearance of parvalbumin (PV) neurons and the formation of glutamic acid decarboxylase 67 (GAD67)-positive puncta around pyramidal neurons in the prefrontal cortex and hippocampus. Whisker trimming, but not dark rearing, decreased the density of PV neurons in the hippocampus at postnatal day 28 (P28). In the prefrontal cortex, whisker trimming and dark rearing decreased the density of PV neurons in layer 5/6 (L5/6) at P28 and in L2/3 at P56, respectively, whereas dark rearing increased the density of PV neurons in L5/6 at P56. Whisker trimming decreased the density of GAD67-positive puncta in CA1 of the hippocampus at both P28 and P56 and in L5/6 of the prefrontal cortex at P28. Dark rearing decreased the density of GAD67-positive puncta in CA1 of the hippocampus and in both L2/3 and L5/6 of the prefrontal cortex at P28, and in L2/3 of the prefrontal cortex at P56. These results demonstrate that somatosensory or visual deprivation causes changes in the PV-interneuronal network in the mouse prefrontal cortex and hippocampus. The results also suggest that the alteration of the PV-interneuronal network, especially in the prefrontal cortex, may contribute to cross-modal plasticity.
Keywords sensory deprivation parvalbumin glutamate decarboxylase (GAD67) prefrontal cortex hippocampus
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2013-06
Volume volume67
Issue issue3
Publisher Okayama University Medical School
Start Page 135
End Page 143
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2013 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23804136
Web of Science KeyUT 000320747900002
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/50870