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目的初步探讨由CX32组成的缝隙连接与癫痫之间的关系。方法利用免疫组织化学方法、West-ernblot方法测定KA致痫后大鼠不同脑区、不同时程的CX32的分布及表达。结果KA致病后大鼠的大脑皮层及海马均有CX32阳性表达。KA注射致痫后的早期CX32的表达明显增强,第3天达到高峰,中、后期其表达逐渐减弱,表达量也逐渐减少。上述变化在海马比皮层明显。结论神经元上的由CX32组成的GJ可能在癫痫的始动和发生上有一定的作用,但在长期的、慢性的癫痫过程中其对癫痫的发生和发展的作用是逐渐减弱的。
Objective To investigate the relationship between gap junction and epilepsy composed of CX32. Methods The distribution and expression of CX32 in different brain regions and different time courses of KA-induced epilepsy rats were detected by immunohistochemistry and West-ernblot method. Results The expression of CX32 in the cerebral cortex and hippocampus of KA-induced rats was positive. The expression of CX32 in early stage of epilepsy induced by KA injection was significantly increased, peaked on the third day, and gradually decreased in the mid and late stages. The expression of CX32 also gradually decreased. The above changes in the hippocampus than the cortex obvious. CONCLUSION: GJ composed of CX32 on neurons may play a role in the initiation and occurrence of epilepsy. However, its effect on the occurrence and development of epilepsy is gradually weakened in long-term and chronic epilepsy.