βCaMKII过量表达损害小鼠海马齿状回区长时程抑制被引量：1

βCaMKII overexpression impairs long-term depression in dentate gyrus of mice

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摘要采用海马齿状回(dentate gyrus,DG)区域特异性过量表达βCaMKII的蛋白修饰转基因小鼠,通过离体电生理技术,研究了βCaMKII高表达对该区域突触可塑性的影响.与对照组相比,转基因小鼠海马齿状回双脉冲抑制反应(paired-pulse depression,PPD)和颗粒细胞的电压—电流曲线(voltage-current curve)没有发生变化,而该区域的长时程抑制(long-term depression,LTD)明显被减弱.实验结果提示,βCaMKII的过量表达不影响小鼠海马齿状回区的突触前递质释放能力和颗粒细胞的被动属性,但损害其长时程抑制.这为进一步研究βCaMKII在学习记忆和突触可塑性中的作用提供了电生理学依据. This experiment was designed to investigate the effects of the XU Hao, WANG Bo, DUAN Yanhong, CAO Xiaohua （Key Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, East China Normal University, Shanghai 200062, China）CaMKII on the longterm depression （LTD） in dentate gyrus（DG）hy using the transgenic mice in which the overexpression of 13CaMKII is restricted to the DG area. Compared to the control group, the paired- pulse depression curve and voltagecurrent response in DG of transgenic mice didn＇t change, but the LTD was significantly reduced. These results suggest that overexpression of the XU Hao, WANG Bo, DUAN Yanhong, CAO Xiaohua （Key Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, East China Normal University, Shanghai 200062, China）3CaMKⅡ may impair the longterm depression without effect on the presynaptic function and passive properties of granule cells in DG area.

作者徐浩王勃段燕红曹晓华

机构地区华东师范大学脑功能基因组学教育部重点实验室

出处《华东师范大学学报（自然科学版）》 CAS CSCD 北大核心 2012年第1期54-62,共9页 Journal of East China Normal University(Natural Science)

基金国家自然科学基金(31070993)

关键词 β钙离子/钙调素依赖的蛋白激酶Ⅱ 海马齿状回长时程抑制 βCaMKⅡdentate gyrus longterm depression

分类号 Q189 [生物学—神经生物学]

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