摘要
目的探讨颞叶癫痫的发病机制。方法取健康雄性SD大鼠制成颞叶癫痫模型,用免疫组织化学和原位杂交技术对匹罗卡品致痫后不同时间点CA_1区的Sema3C mRNA、Np1 mRNA和蛋白表达进行分析。结果在匹罗卡品致痫后7d,实验组CA_1区Sema3C、Np1的表达明显低于对照组(P＜0．01)。结论CA_1区Sema3C、Np1的表达下调可能参与了海马CA_1区内的轴突出芽机制。
Objective To explore the epileptogenesis mechanism of temporal lobe epilepsy（TLE）. Methods Immunohistochemistry and in situ hybridization were used to analyze Sema3C mRNA,Npl mRNA and their protein in CA1 at different time after lithium-chloride and pilocarpine induced TLE. Results 7 days after lithium-chloride and pilocarpine induced TLE,Sema3C and Npl in CAI decreased significantly（P〈0. 01）. Conclusion The down-regulation of Sema3C and Npl in CA1 may be one of the endogenous molecular mechanism of axonal sprouting in CA1.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2007年第1期35-37,共3页
Journal of Apoplexy and Nervous Diseases
