电压门控性钠通道mRNA在海人酸致痫大鼠表达的研究  

The Expression of the mRNAs Encoding Voltage-gated Sodium channel following Kainate-induced Model of Epilepsy

作　　者：谢菊生[1] 肖波[2] 李国良[2] 李静[2] 

机构地区：[1]湖南省郴州市第一人民医院神经内科,423000 [2]中南大学湘雅医院神经内科

出　　处：《脑与神经疾病杂志》2004年第4期259-261,247,共4页Journal of Brain and Nervous Diseases

基　　金：高等学校优秀青年教师教学科研奖励计划(2001-182)

摘　　要：目的:探讨电压门控性钠通道在癫痫发病机制中的作用。方法:采用海人酸颞叶癫痫模型,运用原位杂交技术检测不同时点海马DG区、CA1区、CA2区和CA3区SCN2A、SCN3A mRNA的表达。结果:SCN2A和SCN3AmRNA均表达于海马的DG区、CA1、CA2、CA3区。海人酸致痫后3小时在海马各区表达开始增强,6小时明显增强(P<0.05),12小时达到高峰(P<0.01),24小时开始下降,48小时恢复至正常水平。结论:电压门控性钠通道SCN2AmRNA和SCN3A mRNA的表达增加可能参与了颞叶癫痫急性期的发病。Objective: To explore the roles of the voltage-gated sodium channels in pathogenesis of epilepsy. Methods: Rats were injected with kainite 12 mg/kg intraperitoneally to establish an acute temporal lobe epilepsy model. At 3h, 6h, 12h,24h,48h, 7d after KA induced seizures, by using of in situ hybridization, the SCN2A, SCN3A mRNA were analyzed at different time quantitatively in the the dentate gyrus. areas CA1, CA2 and CA3 of the hippocampus. Results: The expression level of SCN2A and SCN3A mRNA was expressed in the areas CA1 .CA2, CA3 and dentate gyrus of the hippocampus. The amount of them was markedly increased in area CA2 and CA3 of the hippocampus neurons in kainate-treated rats, this increase began in 3h(P<0. 05) , rached a pek at 12h (P<0. 01) and was still persistent at 24h. returning to control values at 48h. Conclusions: The up-regulation of SCN2A and SCN3A mRNA might be concerned with the pathogenesis of temporal lobe epilepsy in acute perios.

关 键 词：海人酸 癫痫动物模型 电压门控 钠通道 

分 类 号：R742.1[医药卫生—神经病学与精神病学]