αCaMKII在前脑过量表达损伤小鼠灵活性学习能力  

Forebrain overexpression of αCaMKII disrupts behavioral flexibility

作　　者：安述明[1] 曾庆文[1] 徐浩[1] 刘汝清[1] 曹晓华[1] 

机构地区：[1]华东师范大学脑功能基因组学教育部重点实验室上海市科学技术委员会重点实验室,上海200062

出　　处：《华东师范大学学报（自然科学版）》2010年第2期111-118,共8页Journal of East China Normal University(Natural Science)

基　　金：国家自然科学基金(30670682)

摘　　要：将3月龄实验小鼠分为αCaMKII-F89G转基因组和同窝野生对照组,进行疲劳转棒实验和Morris水迷宫实验测试.结果显示,转基因组小鼠的体力和运动协调能力与对照组相比无显著的差异;在Morris水迷宫实验的可视平台测试中,转基因鼠的视觉和求生的动机表现正常;在定位航行训练和第一次空间探索测试中,两组鼠在训练时逃避潜伏期及测试中在目标象限探索时间无统计学差异;但是在反向定位空间学习阶段,转基因组在第二、三天逃避潜伏期和距离明显长于同窝对照组(P<0.05).由此认为,αCaMKII在前脑过量表达对小鼠的灵活性学习有损伤作用,推测这种损伤有可能由前脑LTD的缺陷造成的.The αCaMKII-F89G transgenic mice and their littermate controls were subjected to the rotarod test and Morris water maze test.There was no significant difference in motor coordination and ability between these two groups in the rotarod test.In the visible platform test,transgenic mice showed the normal perception,motivation and motor ability.In addition,transgenic mice performed normally in learning and memory in both place navigation training and the 1st spatial probe test.However,compared with wild type mice,transgenic mice spent significantly more time and swam longer distance to reach hidden platform in the 2nd and 3rd day of spatial reversal learning.These results indicate that αCaMKII overexpression in the forebrain can impair spatial reversal learning.The mechanism of the performance deficit may be relevant to disrupted or abolished LTD in the forebrain.

关 键 词：钙/钙调蛋白依赖性蛋白激酶Ⅱ 疲劳转棒实验 MORRIS水迷宫实验 LTD 空间再学习 

分 类 号：Q6[生物学—生物物理学]