摘要
采用马桑内酯大鼠癫痫模型和大鼠高体海马脑片CA1区锥体细胞癌样放电模型，观瘵了非竞争性NMDA受体结抗剂氯胶团对马桑内酯致癌作用的影响．结果发现：实验组大鼠的癫痫发作推迟，程度减轻；痫样脑电图出现的潜伏期延长，波幅下降（P＜0．05）；马桑内酯所致高体海马脑片CA1；区锥体细胞的痫样PS波被抑制：EPSPs幅度下降（P＜0．05）．结果提示：马桑内酯致痫的作用之一可能通过激活交触后膜上NMDA受体，使神经元兴奋性突触传递增强而产生痫样放电．
The effect of ketamine, a noncompetitive inhibitor of NMDA receptor , on the cortartalactone (CL) -induced epilepsy was investisated by using the model of CL-induced rat seisure andepileptiform burst of rat hippocampal CAl region pyramidal cells.The results implied that compared with control group the appearance of rat seisure behaviour was delayed and the degree of seisure was diminished two hours. The tatency of electrocorticogram (ECoG) epileptiform discharge was prolonged significantly, and the amplitude Qf epileptiform ECoG was lowered (P <0. 05). In CA1 region of rat hippocampal slices, the eplleptiform burst numbers (PS) by CL-induction were depressed and so was the amplitude of EPSPs (P<0.05).These results suggest the mechanism of CL-induced epilepsy misht be that it elevated the excita bility of neurones and enhanced the excitatory synaptic transmission by activitihg the NMDA recep tor. The incomplete inhibition of ketamineon CL-induced epilepsy suggests that the receptor is not the only path for CL-induced seizure.
出处
《泸州医学院学报》
1996年第1期15-18,共4页
Journal of Luzhou Medical College
