外伤性癫痫大鼠海马NCAM及GAP-43的动态表达

Kinesis Expression of NCAM and GAP-43 in Hippocampus of Experimental Posttraumatic Epilepsy Rats

目的:动态观察神经细胞黏附分子(NCAM)及颗粒细胞生长相关蛋白-43(GAP-43)在外伤性癫痫(PTE)大鼠海马的表达,探讨有关发病机制。方法:立体定向注射1000nmolFeCl2:于大鼠右侧运动皮层致痫,在不同时间点行为学视频、脑电图监测,用免疫组织化学法检测1、2、3、4周大鼠海马内NCAM及GAP-43的表达。结果:所有大鼠在注射FeCl2后不久记录到癫痫样放电,致痫后1周即可见海马神经元NCAM大量表达,15天达高峰,20天后减少,持续30天;GAP-43表达在5～7天达高峰,2周后明显减少。结论:FeCl2皮层注射可以制成PTE动物模型。与NCAM及GAP-43表达相关的神经元及胶质细胞的动态变化在PTE的发病机制中起重要作用。NCAM表达增加而GAP-43表达减少可能为FeCl2致痫的共同途径。

Objective：To observe the kinesis expression of NCAM and GAP-43 in the Hippocampus of Rats,and discuss the mechanism of pathologic changes and epileptogenesis in the model of posttraumatic epilepsy（PTE）.Methods：Ferrous chloride（FeCl2 1000nmo1）was injected into the motor cortex of rats via stereotactic technique.Behavior was observed and EEG were recorded following injection.Dynamic change of the expression of NCAM and GAP-43 in hippocampus after epileptic seizure in 1w,2w,3w and 4w by using immunohistochemcal methods.Results：All of the rats developed epileptiform discharges soon after FeCl2-injection.Compared with the control group,the expression of NCAM were increased in 1w,and rose to the peak in 15d,decreased significantly in 3w later ;the expression of GAP-43 rose to the peak in 5～7d,and there were no significance in 14 and 21 or 30 days later.Conclusion：The intracortical injection of 1000nmol FeCl2,induced model is an ideal animal PTE model.The changes of the kinesis expression of NCAM and GAP-43 in the Hippocampus concerned with the mechanism of pathologic changes and epileptogenesis in this model.