癫痫大鼠内嗅皮层神经元GABAA受体功能的研究

目的介绍建立氯化锂-匹鲁卡品致痫大鼠模型的方法,并且通过全细胞膜片钳记录,初步研究其内嗅皮层神经元GABAA受体功能。方法将所有SD大鼠随机分为对照组和实验组。实验组大鼠腹腔注射氯化锂以及匹鲁卡品,对照组注射生理盐水,观察其行为学特征,并用全细胞膜片钳记录GABAA受体电流的衰减趋势。结果与对照组相比,实验组癫痫大鼠内嗅皮层神经元的GABAA受体电流的衰减加剧。方差检验进行组间分析,分组的作用是有差异的(P<0.001),;固定时间,对每个时间点上的处理组和对照组进行t检验,分组都有统计学意义(P<0.001)。结论锂-匹罗卡品致痫大鼠内嗅皮层神经元的GABAA受体电流衰减的加剧,说明了锂、匹罗卡品造成大鼠癫痫的可能原因,也提示了GABAA受体参与了癫痫发作以及癫痫发作后的脑损伤。

The function study of entorhinal cortex neuron GABAA receptor in an epilepsia rat model

Objective Established the lithium chloride-pilocarpine inducing epilepsia rat model,and initially study about the entorhinal cortex neuron GABAA receptor by patch clamp of whole-cell mode.Methods The SD rats were divided into control group and experiment group randomly.Intraperitoneal injection of lithium chloride-pilocarpine have been used in experiment group,and physiologic saline in control group.Observed the ethology characteristic and recorded the attenuation tendency of GABAa receptor electric current in whole cell mode.Results The electric current attenuation tendency of GABAA Receptor of Epilepsia Rat greatly intensify in the experiment group.The group diveded have significant difference by variance test and interclass analyse(P<0.05),and the datas of every point of time in experiment group and control group also have significant difference by t-text analyse(P<0.05).Conclusion The electric current attenuation tendency of Entorhinal Cortex Neuron GABAA Receptor of lithium chloride-pilocarpine inducing epilepsia rat have intensified.This phenomenon could be the possible mechanism of lithium chloride-pilocarpine inducing epilepsia rat and hint that GABAA receptor may contribute to the epileptic attack and brain injured after epileptic attack.