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βCaMKII过量表达损害小鼠海马齿状回区长时程抑制

徐浩 王勃 段燕红 曹晓华

徐浩, 王勃, 段燕红, 曹晓华. βCaMKII过量表达损害小鼠海马齿状回区长时程抑制[J]. 华东师范大学学报(自然科学版), 2012, (1): 54-62.
引用本文: 徐浩, 王勃, 段燕红, 曹晓华. βCaMKII过量表达损害小鼠海马齿状回区长时程抑制[J]. 华东师范大学学报(自然科学版), 2012, (1): 54-62.
XU Hao, WANG Bo, DUAN Yan-hong, CAO Xiao-hua. βCaMKII overexpression impairs long-term depression in dentate gyrus of mice[J]. Journal of East China Normal University (Natural Sciences), 2012, (1): 54-62.
Citation: XU Hao, WANG Bo, DUAN Yan-hong, CAO Xiao-hua. βCaMKII overexpression impairs long-term depression in dentate gyrus of mice[J]. Journal of East China Normal University (Natural Sciences), 2012, (1): 54-62.

βCaMKII过量表达损害小鼠海马齿状回区长时程抑制

详细信息
  • 中图分类号: Q189

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

  • 摘要: 采用海马齿状回(dentate gyrus, DG)区域特异性过量表达CaMKII的蛋白修饰转基因小鼠,通过离体电生理技术,研究了CaMKII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,CaMKII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CaMKII在学习记忆和突触可塑性中的作用提供了电生理学依据.
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出版历程
  • 收稿日期:  2011-02-01
  • 修回日期:  2011-05-01
  • 刊出日期:  2012-01-25

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