目的:探讨钠离子通道功能的改变在大脑皮质发育障碍性癫痫形成中的作用。方法:采用给孕鼠腹腔注射卡莫司汀的方法制作子代广泛型皮质发育障碍模型。急性分离大鼠海马CA1区神经元,运用全细胞膜片钳技术记录电压依赖性钠电流,并将模型组与对照组进行比较。结果:皮质发育障碍模型组CA1区神经元钠电流激活的电压依赖性向超极化方向偏移,失活的电压依赖性向去极化方向偏移,窗口钠电流较对照组明显增大(P〈0.05)。模型组失活后的恢复时间常数较对照组明显缩短(P〈0.05)。结论:电压依赖性钠通道功能的改变可能与皮质发育障碍癫痫易感性增高有关。
AIM: To study the changes in function of voltage - dependent sodium channel and the epileptogenic mechanisms in models with cortical developmental disabilities. METHODS : The animal models of cortical developmental disabilities were established by BCNU - exposure in uterus. Voltage - dependent sodium currents were recorded in acutely isolated CA1 pyramidal neurons using the whole - cell patch - clamp technique. Their properties were analyzed and compared to normal control group. RESULTS : The voltage dependence of activation for sodium current shifted to more hyperpolarized potentials. In combination with a shift in the voltage dependence of inactivation to more depolarized potentials, it resulted in a window current which was significantly increased in the BCNU - exposed neurons ( P 〈 0. 05 ). The recovery time constant for sodium currents was significantly shorter in neurons of modal group (P 〈 0. 05). CONCLUSION: The functional abnormalities of voltage - dependent sodium channel contribute to the enhanced excitability and decreased seizure threshold associated with cortical developmental disabilities in BCNU -exposed rats.