Bai Zhan-Tao, Zhao Rong, Zhang Xu-Ying, Chen Jin, Liu Tong, Ji Yong-Hua
Graduate School of the Chinese Academy of Sciences, Institute of Physiology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, PR China.
Exp Neurol. 2006 Jan;197(1):167-76. doi: 10.1016/j.expneurol.2005.09.006. Epub 2005 Oct 17.
In the present study, the susceptibility to rat epileptic seizures induced by the intrahippocampal administration of BmK I, a modulator of sodium channels purified from the venom of Chinese scorpion, has been investigated. The results showed that the strong epileptic behaviors and discharges in the hippocampus were evoked by BmK I dose-dependently. The hippocampal c-Fos expression displayed two peak waves in a specific spatio-temporal pattern elicited by BmK I. The whole cell patch clamp recordings showed that the inactivation of sodium currents in rat cultured hippocampal neurons was prolonged significantly by BmK I, and restored partially after washing. These results indicated that the rat hippocampus is a susceptible target for the proconvulsant effects of BmK I, and the induction of epileptic seizures may be ascribed to the modulation of BmK I on the inactivation of voltage-gated sodium channels distributing in the rat hippocampal neurons.
在本研究中，已对从中国蝎子毒液中纯化的钠通道调节剂BmK I经海马内给药诱导大鼠癫痫发作的易感性进行了研究。结果表明，BmK I剂量依赖性地诱发了强烈的癫痫行为和海马放电。BmK I引发的海马c-Fos表达以特定的时空模式呈现两个峰值波。全细胞膜片钳记录显示，BmK I显著延长了大鼠培养海马神经元中钠电流的失活，冲洗后部分恢复。这些结果表明，大鼠海马是BmK I促惊厥作用的敏感靶点，癫痫发作的诱导可能归因于BmK I对分布在大鼠海马神经元中的电压门控钠通道失活的调节。
