Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex

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....

Full description

Saved in:
Bibliographic Details
Main Authors: Hiroshi Ueno, Shunsuke Suemitsu, Yosuke Matsumoto, Motoi Okamoto
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2015/753179
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832564736329252864
author Hiroshi Ueno
Shunsuke Suemitsu
Yosuke Matsumoto
Motoi Okamoto
author_facet Hiroshi Ueno
Shunsuke Suemitsu
Yosuke Matsumoto
Motoi Okamoto
author_sort Hiroshi Ueno
collection DOAJ
description 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.
format Article
id doaj-art-261a5a28a61b4a10950db9f4f6a2292b
institution Kabale University
issn 2090-5904
1687-5443
language English
publishDate 2015-01-01
publisher Wiley
record_format Article
series Neural Plasticity
spelling doaj-art-261a5a28a61b4a10950db9f4f6a2292b2025-02-03T01:10:18ZengWileyNeural Plasticity2090-59041687-54432015-01-01201510.1155/2015/753179753179Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal CortexHiroshi Ueno0Shunsuke Suemitsu1Yosuke Matsumoto2Motoi Okamoto3Department of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, JapanDepartment of Psychiatry, Kawasaki Medical University, Kurashiki 701-0192, JapanDepartment of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, JapanDepartment of Medical Technology, Graduate School of Health Sciences, Okayama University, Okayama 700-8558, JapanEarly 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.http://dx.doi.org/10.1155/2015/753179
spellingShingle Hiroshi Ueno
Shunsuke Suemitsu
Yosuke Matsumoto
Motoi Okamoto
Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
Neural Plasticity
title Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
title_full Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
title_fullStr Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
title_full_unstemmed Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
title_short Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex
title_sort sensory deprivation during early postnatal period alters the density of interneurons in the mouse prefrontal cortex
url http://dx.doi.org/10.1155/2015/753179
work_keys_str_mv AT hiroshiueno sensorydeprivationduringearlypostnatalperiodaltersthedensityofinterneuronsinthemouseprefrontalcortex
AT shunsukesuemitsu sensorydeprivationduringearlypostnatalperiodaltersthedensityofinterneuronsinthemouseprefrontalcortex
AT yosukematsumoto sensorydeprivationduringearlypostnatalperiodaltersthedensityofinterneuronsinthemouseprefrontalcortex
AT motoiokamoto sensorydeprivationduringearlypostnatalperiodaltersthedensityofinterneuronsinthemouseprefrontalcortex