Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
Identifieur interne : 000570 ( Main/Merge ); précédent : 000569; suivant : 000571Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
Auteurs : Hiroshi Ueno [Japon] ; Shunsuke Suemitsu [Japon] ; Yosuke Matsumoto [Japon] ; Motoi Okamoto [Japon]Source :
- Neural Plasticity [ 2090-5904 ] ; 2015.
Abstract
Early loss of one sensory system can cause improved function of other sensory systems. However, both the time course and neuronal mechanism of cross-modal plasticity remain elusive. Recent study using functional MRI in humans suggests a role of the prefrontal cortex (PFC) in cross-modal plasticity. Since this phenomenon is assumed to be associated with altered GABAergic inhibition in the PFC, we have tested the hypothesis that early postnatal sensory deprivation causes the changes of inhibitory neuronal circuit in different regions of the PFC of the mice. We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices. The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6). Moreover, the density of CR neurons was higher in L2/3 in sensory deprived mice compared to intact mice. These changes were more prominent at P56 than at P28. These results suggest that long-term sensory deprivation causes the changes of intracortical inhibitory networks in the PFC and the changes of inhibitory networks in the PFC may contribute to cross-modal plasticity.
Url:
DOI: 10.1155/2015/753179
PubMed: 26161272
PubMed Central: 4487934
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id="I1">Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558</wicri:regionArea><wicri:noRegion>Okayama 700-8558</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="I2">Department of Medical Technology, Kawasaki College of Allied Health Professions, Okayama 701-0194, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Medical Technology, Kawasaki College of Allied Health Professions, Okayama 701-0194</wicri:regionArea><wicri:noRegion>Okayama 701-0194</wicri:noRegion></affiliation></author><author><name sortKey="Suemitsu, Shunsuke" sort="Suemitsu, Shunsuke" uniqKey="Suemitsu S" first="Shunsuke" last="Suemitsu">Shunsuke Suemitsu</name><affiliation wicri:level="1"><nlm:aff id="I3">Department of Psychiatry, Kawasaki Medical University, Kurashiki 701-0192, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Psychiatry, Kawasaki Medical University, Kurashiki 701-0192</wicri:regionArea><wicri:noRegion>Kurashiki 701-0192</wicri:noRegion></affiliation></author><author><name sortKey="Matsumoto, Yosuke" sort="Matsumoto, Yosuke" uniqKey="Matsumoto Y" first="Yosuke" last="Matsumoto">Yosuke Matsumoto</name><affiliation wicri:level="1"><nlm:aff id="I4">Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558</wicri:regionArea><wicri:noRegion>Okayama 700-8558</wicri:noRegion></affiliation></author><author><name sortKey="Okamoto, Motoi" sort="Okamoto, Motoi" uniqKey="Okamoto M" first="Motoi" last="Okamoto">Motoi Okamoto</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558</wicri:regionArea><wicri:noRegion>Okayama 700-8558</wicri:noRegion></affiliation></author></analytic><series><title level="j">Neural Plasticity</title><idno type="ISSN">2090-5904</idno><idno type="eISSN">1687-5443</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Early loss of one sensory system can cause improved function of other sensory systems. However, both the time course and neuronal mechanism of cross-modal plasticity remain elusive. Recent study using functional MRI in humans suggests a role of the prefrontal cortex (PFC) in cross-modal plasticity. Since this phenomenon is assumed to be associated with altered GABAergic inhibition in the PFC, we have tested the hypothesis that early postnatal sensory deprivation causes the changes of inhibitory neuronal circuit in different regions of the PFC of the mice. We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices. The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6). Moreover, the density of CR neurons was higher in L2/3 in sensory deprived mice compared to intact mice. These changes were more prominent at P56 than at P28. 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