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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 expression of neural cell adhesion molecule (NCAM) and granule cell growth associated protein-43 (GAP-43) in the hippocampus of rats with traumatic epilepsy (PTE) and to explore the pathogenesis. METHODS: Stereotaxic injection of 1000 nmol FeCl2: induced epilepsy in the right motor cortex of rats. The behavioral video and EEG at different time points were used to detect NCAM in the hippocampus, GAP-43 expression. Results: Epileptiform discharges were recorded in all rats shortly after injection of FeCl2. The NCAM expression in hippocampal neurons was observed at 1 week after epileptic seizure, reaching the peak at 15 days and decreasing after 20 days for 30 days. The expression of GAP- 7 days peak, significantly reduced after 2 weeks. Conclusion: FeCl2 injection can be used to make PTE animal model. The dynamic changes of neurons and glial cells related to NCAM and GAP-43 expression play an important role in the pathogenesis of PTE. The increase of NCAM expression and the decrease of GAP-43 expression may be the common pathway of FeCl2 induced epilepsy.