惊厥对神经元缝隙连接蛋白基因表达的影响  

Effect of Seizures on Neuronal Gap Junction Gene Expression

作　　者：张月华[1] 张国荣[1] 单巍松[1] 王朝晖[1] 吴希如[1] 

机构地区：[1]北京医科大学第一医院儿科,北京100034

出　　处：《基础医学与临床》1999年第3期80-84,共5页Basic and Clinical Medicine

基　　金：卫生部科研基金!94-1-260

摘　　要：神经元之间的缝隙连接蛋白Cx32是形成电突触的结构基础，电突触参与惊厥时神经元的同步化放电过程。为探讨惊厥对脑内神经元Cx32基因表达的影响，以遗传性癫痫易感大鼠P77PMC为模型，采用原位杂交的方法观察P77PMC大鼠听源性惊厥后脑内Cx32基因表达的变化。原位杂交结果显示：惊厥后在大脑皮层，海马脑区Cx32mRNA表达呈时间依赖性上调，惊厥后4h表达量明显增加，24h达高峰，结果提示：惊厥能上调神经元Cx32mRNA表达，从而可能使神经元之间的电突触联系增加，有利于神经元的同步化放电，加重惊厥的发生发展。Neuronal gap junction protein Cx32 is the structural basis for electrical synapse.Electrical synapse plays an inportant role in the synchronization of neuronal discharges.In order to investigate the effect of seizures on neuronal Cx32 gene expression, genetical epilepsy prone rat P77PMC was used as a model,changes of Cx32 gene expression in the brain was observed by using in situ hybridization after audiogenic seizure.The results showed that:after audiogenic seizure,in cerebratl cortex and hippocampus, Cx32 mRNA expression showed time-dependent increase, it significantly elevated at 4h, reached a peak at 24h. The results indicated that seizures could upregulate neuronal Cx32 mRNA expression and may increase the number of electrical synapses between neurons. This benifits the synchronization of neuronal discharges and deteriorates the development of seizures.

关 键 词：惊厥 神经元 缝隙连接蛋白 电突触 癫痫 

分 类 号：R742.1[医药卫生—神经病学与精神病学]