权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

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

小鼠视觉皮层暗育效应评价及发育可塑性相关分子鉴定研究

基本信息

批准号：
11680814
负责人：
MATAGA Nobuko
金额：
$ 2.3万
依托单位：
The Institute of Physical and Chemical Research
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2001
项目状态：
已结题

项目摘要

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.

小猫视皮层的经验依赖性可塑性是一个有据可查的现象，然而，这种可塑性的分子和细胞基础仍然未知。最近，我们报道了眼优势（OD）的可塑性水平，甚至可以估计在小鼠视觉皮层的双眼区。在这项研究中，我们首先研究是否黑暗饲养（DR）延迟功能的关键期OD可塑性在小鼠视觉皮层在其他物种。1)成年C57 bl/6小鼠提出的完全没有视觉保留敏感性，短暂的单眼剥夺（MD）的年龄时，轻饲养的同行（LD）不再塑料。2)谷氨酸和γ-氨基丁酸含量在DR组与LD组相近。3)与LD相比，DR双眼区小清蛋白阳性中间神经元的发育受到阻碍。本研究首次报道了用小鼠视皮层进行DR实验，发现谷氨酸脱羧酶（GAD 65）基因敲除小鼠（KO）中一个依赖于活动的即刻早期基因（egr 1）的表达上调，损害了OD可塑性。为了了解β-1是否参与OD可塑性，我们检测了β-1 KO中的MD效应。虽然认为OD 1是OD可塑性的一个必需基因，但在关键期，当小鼠单眼闭上4d时，在OD 1 KO小鼠的视皮层中发现了正常的OD偏移。为了鉴定用于调节OD可塑性的候选分子，我们使用tPA KO小鼠进行蛋白质组分析，这是OD可塑性破坏的第二种动物模型。我们发现，膜联蛋白VI的表达模式是完全不同的野生型和tPA KO后，4天的MD在关键时期。需要进一步的实验来了解该蛋白质与OD可塑性之间的关系。