【摘 要】
：
癫痫往往伴有学习、记忆、行为等认知障碍.主要表现为智力、记忆力及学习能力下降、注意困难,行为障碍等.长期反复的痫性发作所导致的并发症—学习记忆减退在临床上很常见,尤其是儿童和成人的颞叶癫痫.在癫痫动物模型的实验研究中同样发现痫性发作可以直接影响认知功能.但是癫痫导致认知功能障碍的机制仍然存在争议.有研究称痫性放电可以干扰正常神经元间的信息传递,导致一过性认知损害.也有研究报告在癫痫动物模型上观察到
【机 构】
：
上海交通大学医学院仁济医院神经科 上海交通大学医学院生命学院神经科学研究所
【出 处】
：
中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
癫痫往往伴有学习、记忆、行为等认知障碍.主要表现为智力、记忆力及学习能力下降、注意困难,行为障碍等.长期反复的痫性发作所导致的并发症—学习记忆减退在临床上很常见,尤其是儿童和成人的颞叶癫痫.在癫痫动物模型的实验研究中同样发现痫性发作可以直接影响认知功能.但是癫痫导致认知功能障碍的机制仍然存在争议.有研究称痫性放电可以干扰正常神经元间的信息传递,导致一过性认知损害.也有研究报告在癫痫动物模型上观察到导致学习记忆减退的一个可能的原因是神经元过度的兴奋导致细胞死亡.然而,仍有很多关于癫痫动物模型的研究并没有发现反复的痫性发作会引起明显的细胞死亡,而是发现学习记忆的损伤与神经元突触传递和突触可塑性相关,即发现学习记忆的损伤伴随着神经细胞膜上的受体表达或功能的改变.LTP是突触可塑性的一种形式,被认为是哺乳动物记忆形成的生理学模型.在癫痫病人和癫痫动物模型的研究中都发现海马神经元LTP的显著减退甚至消失.目前在多种癫痫动物模型上的许多研究都发现突触后膜上谷氨酸受体的变化在癫痫导致学习记忆减退的机制中发挥作用.但是突触前膜上受体的变化是否参与了癫痫导致的记忆损伤和LTP的减退还没有报道.我们建立了匹罗卡品—氯化锂(lithium chloride-pilocarpine,LiCl-PILO)联合诱导的成年小鼠癫痫模型,并且在体观察其恐惧记忆的形成和离体脑片LTP的诱导情况.我们发现在恐惧记忆衰减同时,LTP诱导的损伤是通过突触前的机制所引起的.
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