Study for evaluation of dark-rearing effects in mouse visual cortex and for identification of developmental plasticity related molecules

Experience-dependent plasticity in the kitten visual cortex is a well-documented phenomenon，however，the molecular and cellular basis for this plasticity remains unknown.Recently we have reported that ocular dominance(OD)plasticity level can be estimated even in the binocular zone of mouse visual cortex.In this study，we first examined whether dark-rearing(DR)delays the functional critical period of OD plasticity in mouse visual cortex as in other species.1)Adult C57bl/6mice raised in the total absence of vision retained sensitivity to brief monocular deprivations(MD)at an age when light-reared counterparts(LD)were no longer plastic.2)Glutamate and GABA contents in DR adult animal were similar to LD.3)development of parvalbumin positive interneurons was retarded in the binocular zone of DR compared to LD.These results indicate that the critical period is prolonged in older animals by DR.This is the first report about DR experiment using mouse visual cortex.Previous our finding indicates that an activity-dependent immediate early gene(Egr1)expression was up-regulated in glutamic acid decarboxylase(GAD65)knockout mice(KO)，which impaired OD plasticity.To know whether egr-1is involved in OD plasticity，we examined MD effect in egr-1KO.Although egr-1is thought to be an essential gene for OD plasticity，normal OD shift was found in egr-1KO mouse visual cortex when their one eye was closed for 4·days during ehe critical period.To identify candidate molecules for the regulation of OD plasticity，we performed the proteome analysis using tPA KO mice，which is second animal model with a disruption in OD plasticity。We found that annexine VI expression pattern was completely different between wt and tPA KO after4-days MD during the critical period.Further experiments will be necessary to know the relationship between this protein and OD plasticity.

Experience-dependent plasticity in the kitten visual cortex is a well-documented phenomenon, however, the molecular and cellular basis for this plasticity remains unknown. Recently we have reported that ocular dominance (OD) plasticity level can be estimated even in the binocular zone of mouse visual cortex. In this study, we first examined whether dark-rearing (DR) delays the functional critical period of OD plasticity in mouse visual cortex as in other species. 1) Adult C57bl/6 mice raised in the total absence of vision retained sensitivity to brief monocular deprivations (MD) at an age when light-reared counterparts (LD) were no longer plastic. 2) Glutamate and GABA contents in DR adult animal were similar to LD. 3) development of parvalbumin positive interneurons was retarded in the binocular zone of DR compared to LD. These results indicate that the critical period is prolonged in older animals by DR. This is the first report about DR experiment using mouse visual cortex.Previous our finding indicates that an activity-dependent immediate early gene (egr1) expression was up-regulated in glutamic acid decarboxylase (GAD65) knockout mice (KO), which impaired OD plasticity. To know whether egr-1 is involved in OD plasticity, we examined MD effect in egr-1 KO. Although egr-1 is thought to be an essential gene for OD plasticity, normal OD shift was found in egr-1 KO mouse visual cortex when their one eye was closed for 4・days during ehe critical period. To identify candidate molecules for the regulation of OD plasticity, we performed the proteome analysis using tPA KO mice, which is second animal model with a disruption in OD plasticity. We found that annexine VI expression pattern was completely different between wt and tPA KO after 4-days MD during the critical period. Further experiments will be necessary to know the relationship between this protein and OD plasticity.