钙离子／钙调蛋白激酶Ⅱ在癫痫中的作用机制  

Advances in Research on the Mechanism of Calcium/calmodulin-dependent Protein Kinase Ⅱ in Epilepsy

作　　者：徐硕妍 王千慧[2] 郭凤[2] 

机构地区：[1]中国医科大学七年制临床医学,沈阳110122 [2]中国医科大学药学院药物毒理学教研室,沈阳110122

出　　处：《中国医科大学学报》2017年第7期577-581,共5页Journal of China Medical University

基　　金：国家自然科学基金(81001429,81471323);辽宁省大学生创新创业训练项目(2015039)

摘　　要：钙离子/钙调蛋白激酶Ⅱ(CaMKⅡ)是一种多功能丝氨酸/苏氨酸蛋白激酶。CaMKⅡ在神经递质、细胞代谢和突触重塑性等方面参与调节,在诸多神经系统疾病中发挥极其重要的作用。CaMKⅡα特异性定位于兴奋性神经元中,一直被认为是研究治疗癫痫的关键所在。体内和体外不同癫痫模型出现CaMKⅡ的活性下降。本文从CaMKⅡ的生物学分类、结构与特性以及CaMKⅡ在癫痫中的作用方面进行综述,为深入研究癫痫病理过程及癫痫药物治疗提供新的理论依据。Calcium/calmodulin-dependent protein kinase Ⅱ （CaMK Ⅱ ） is a muhifuncfional serine/threonine protein kinase. It plays a vital role in the regulation of , cell metabolism, and synaptic plasticity, as well as in many diseases of the nervous system. As CaMK Ⅱ alpha is specifically located at excitatory neurons ,it has long been regarded as crucial for the treatment of epilepsy. CaMK Ⅱ shows decreased activity after seizures in different in vivo and in vitro models of epilepsy. This article provides a new theoretical basis for fixrther research on the pathological process of epilepsy and its treatment, by exploring several recent experimental studies on CaMK Ⅱ and epilepsy.

关 键 词：钙离子/钙调蛋白激酶Ⅱ 癫痫 细胞特异性 共定位效应 突触重塑性 

分 类 号：R99[医药卫生—毒理学]