βCaMKII过量表达损害小鼠海马齿状回区长时程抑制

被引:1
作者
徐浩
王勃
段燕红
曹晓华
机构
[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脑功能基因组学重点实验室
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;
D O I
暂无
中图分类号
R338 [神经生理学];
学科分类号
100115 [医学神经生物学];
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.
引用
收藏
页码:54 / 62
页数:9
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