1型脆性X智力低下基因敲除鼠锥体神经元钠通道电生理特性研究

Electrophysiological characteristics of sodium channel in pyramidal neurons in fragile X mental retardation 1 knockout mice

目的 通过检测1型脆性X智力低下基因（FMR1）敲除型（KO）鼠和野生型（WT）鼠海马锥体神经元钠电流的电生理学变化,探讨神经元兴奋性改变在FMR1 KO鼠癫痫形成中的作用.方法 采用急性分离技术获得FMR1 KO鼠与WT鼠锥体神经元,用膜片钳技术记录钠离子通道的激活、失活及恢复等电生理特性.结果 FMR1 KO鼠锥体神经元电流密度为0.2932±0.106（nA/pF）;高于WT鼠电流密度0.1260±0.054（nA/pF）,P〈0.05,差异有统计学意义.KO鼠激活、失活及恢复等电生理特性与WT鼠相比差异无统计学意义.结论 锥体神经元电流密度增加导致的兴奋性增高可能使得FMR1 KO鼠癫痫易感性增加.

Objective To determine the electrophysiological changes of sodium current in hippocampal pyramidal neurons in fragile X mental retardation 1（FMR1）knockout（KO）mice and wild-type （WT）mice,and to investigate the effect of the change of neuronal excitability on epilepsy in FMR1 KO mice. Methods The acute isolated technique was used to obtain the pyramidal neurons in FMR1 KO mice and WT mice. The electrophysiological characteristics,such as the activation,inactivation and recovery of sodium channels were recorded by patch clamp technique. Results The current density of pyramidal neurons in FMR1 KO mice was 0.2932 ± 0.106（nA/pF）,which was higher than 0.1260 ± 0.054（nA/pF）of WT mice,P〈0.05,and the difference was statistically significant. There were no statistically significant differences in the electrophysiological characteristics of activation,inactivation and recovery between the KO mice and WT mice. Conclusion The enhanced excitability of pyramidal neurons caused by increased current density might contribute to the susceptibility of epilepsy in FMR1 KO mice.