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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。
OBJECTIVE: To introduce a method of establishing a model of epileptic rat induced by lithium chloride-pilocarpine, and to study the function of GABAA receptor of entorhinal cortex neurons through whole-cell patch-clamp recording. Methods All SD rats were randomly divided into control group and experimental group. Rats in the experimental group were injected intraperitoneally with lithium chloride and pilocarpine. The control group was injected with normal saline, and the behavioral characteristics were observed. The attenuation trend of GABAA receptor current was recorded by whole-cell patch-clamp. Results Compared with the control group, the decay of GABAA receptor currents in the entorhinal cortex neurons in the experimental group increased. Variance test was used to analyze the differences between the two groups (P <0.001). At fixed time, t-test was performed on the treatment group and the control group at each time point with statistical significance (P <0.001) ). Conclusion The aggravation of GABAA receptor current decay in the entorhinal cortex neurons of lithium-pilocarpine-induced epileptic rats illustrates the possible causes of epilepsy in rats induced by lithium and pilocarpine, and also suggests that GABAA receptor is involved in epilepsy Seizures and brain damage after seizures.