【摘要】 目的初步探讨由CX36组成的GJ在癫痫发病中的作用。方法建立36只大鼠KA注射致痫动物模型,分奎宁组、甘珀酸组和对照组(每组12只),在在体上分别局部给予奎宁、甘珀酸和生理盐水,用脑电图仪观测用药前后每组中大鼠皮层脑电活动的变化情况。利用免疫组织化学方法、Western blot方法测定各实验组致痫大鼠不同脑区CX36的分布及表达。结果奎宁组及甘珀酸组异常脑电发作次数、平均振幅给药前后比较均有显著性差异(P<0.01);生理盐水组则无显著性差异(P>0.05)。奎宁组给药前后异常脑电发作次数和波幅的变化值与甘珀酸组相比无显著性差异(P>0.05)。KA致痫后大鼠的大脑皮层及海马CX36含量明显增多,且在海马中的变化比皮层明显,但无统计学意义(P>0.05)。奎宁组及甘珀酸组CX36的表达量低于对照组(P<0.01),但奎宁组与甘珀酸组两组CX36的表达量无显著性差异(P>0.05)。结论神经元上的由CX36组成的缝隙连接可能在癫痫发病初期占有主导地位。更多还原

【Abstract】 Objective To investigate the effect of gap junction via CX36 on seizure activity in rats.Methods 36 kainic acid-induced experimental epilepsy rats were medially divided into quinine group,carbenoxolone group and control group.Quinine,carbenoxolone and saline was topically administered in vivo.Electroencephalogram was introduced to record electrical activity of rat cortex before and after administering drug.The expression and distribution of CX36 in different encephalic regions in each group was determined by using immunohistochemistry and western blotting.Results The frequency and amplitude of abnormal electrical activity has significant difference before and after administering drug in quinine group and carbenoxolone group individually(P<0.01).However,there was no significant difference in saline group(P>0.05).The change of frequency and amplitude of abnormal electrical activity before and after administering drug had significant difference comparing quinine group with carbenoxolone group(P>0.05).The expression of CX36 in cortex and hippocampus of KA-induced experimental epilepsy rats significantly increased.The change in hippocampus was more obvious than in cortex.However,there was no significant difference(P>0.05).The expression of CX36 was lower in quinine group and in carbenoxolone than that in control group.However,there was no significant difference in quinine group and in carbenoxolone group(P>0.05).Conclusion Gap-junction via CX36 in neuron may play critical role in the initial stage of seizure activity.更多还原