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近年的研究提示,神经细胞内Ca~(2+)超载是某些神经元痫样放电产生的起始因素。但Ca~(2+)在马桑内酯(Coriaria Lactone,CL)致痫机制中的作用尚不清楚。本文选用L—型电压依赖性Ca~(2+)通道阻断剂硝苯吡啶和NMDA受体拮抗剂氯胺酮,分别阻断两类不同性质的Ca~(2+)通道,从整体、细胞、基因三个水平来系统地分析Ca~(2+)在CL致痫中的作用。
Recent studies have shown that Ca ~ (2+) overload in nerve cells is the starting factor for some neuronal epileptiform discharges. However, the role of Ca ~ (2+) in the mechanism of epileptiform induced by Coriaria Lactone (CL) is unclear. In this paper, L-type voltage-dependent Ca 2+ channel blocker nifedipine and NMDA receptor antagonist ketamine were used to block two types of Ca 2+ channels with different properties, Gene three levels to systematically analyze the role of Ca ~ (2+) in the epilepsy induced by CL.