αCaMKII过量表达增强小鼠岛叶皮层兴奋性突触传递

摘要/Abstract

摘要： 为了研究αCaMKII在小鼠前脑过量表达对岛叶皮层兴奋性锥体细胞基本电生理特性和突触传递的影响，利用脑片膜片钳技术研究αCaMKII-F89G转基因小鼠岛叶皮层锥体细胞的基本电生理性质及突触传递.结果显示：野生型和αCaMKII-F89G转基因型小鼠岛叶皮层锥体细胞在静息膜电位，动作电位及电流—电压曲线方面没有显著性差异；在突触传递中，野生型鼠与转基因鼠的自发兴奋性突触后电流和微小兴奋性突触后电流的幅度差异显著，而频率没有显著性差异；此外，两组小鼠的双脉冲易化（PPF）曲线也没有显著性差异.由此得出结论，αCaMKII在前脑特异性过量表达可能不改变岛叶皮层锥体细胞基本电生理特性和突触前递质释放能力；αCaMKII过量表达提高自发兴奋性突触后电流幅度可能是通过突触AMPA 和（或）NMDA受体介导的.

关键词: &alpha, CaMKII, 岛叶皮层, 兴奋性突触后电流

Abstract: The experiment was designed to study basic electrophysiological characteristics and basal synaptic transmission of insular pyramidal cells in αCaMKII forebrain overexpression mice by patch clamping. The basic electrophysiological results showed that there were no significant differences in the resting membrane potential, action potential and I-V curve of pyramidal cells in insular cortex between wild type and transgenic mice. No significant difference was measured in the frequency of sEPSCs and mEPSCs. However, compared to the wild type mice, transgenic mice exhibited augmented amplitude of sEPSCs and mEPSCs. There was also no significant difference in PPF curve. The results suggested that forebrain specific overexpression of αCaMKII did not change the basic electrophysiological characteristics and presynaptic transmitter release in insular cortex. The influence of αCaMKII overexpression on the amplitude of EPSCs may be mediated by postsynaptic receptors.

Key words: αCaMKII, Insular cortex, EPSCs

中图分类号:

Q427

刘汝清，段燕红，曹晓华. αCaMKII过量表达增强小鼠岛叶皮层兴奋性突触传递[J]. 华东师范大学学报(自然科学版), 2011, 2011(4): 94-103,123.

LIU Ru-qing, DUAN Yan-hong, CAO Xiao-hua. αCaMKII overexpressions enhance excitatory synaptic transmission in insular cortex of mice[J]. Journal of East China Normal University(Natural Sc, 2011, 2011(4): 94-103,123.

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