title: Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex.
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.
authors.affiliation: Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan ; Department of Medical Technology, Kawasaki College of Allied Health Professions, Okayama 701-0194, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ueno
authors.affiliation: Department of Psychiatry, Kawasaki Medical University, Kurashiki 701-0192, Japan.
authors.forename: Shunsuke
authors.initials: S
authors.lastname: Suemitsu
authors.affiliation: Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan.
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Matsumoto
authors.affiliation: Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, Japan.
authors.forename: Motoi
authors.initials: M
authors.lastname: Okamoto
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D064032:Calbindin 2 / Q000378:metabolism; D064026:Calbindins / Q000378:metabolism; D002452:Cell Count; D059330:GABAergic Neurons / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D007395:Interneurons / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009473:Neuronal Plasticity; D010320:Parvalbumins / Q000378:metabolism; D017397:Prefrontal Cortex / Q000166:cytology* / Q000254:growth & development / Q000378:metabolism; D012683:Sensory Deprivation / Q000502:physiology*
chemical_list: D064032:Calbindin 2; D064026:Calbindins; D010320:Parvalbumins