摘要
目的:探讨神经元异位自发放电的产生机制.方法:分离背根单纤维,引导来自损伤背根节(DRG)神经元的异位自发放电,观察Ca(2+)和K+离子浓度变化及有关通道阻断剂对其的影响.结果:细胞外Ca(2+)浓度升高及应用咖啡因可抑制异位自发放电,降低其放电数;而低钙作用时则相反,使放电数增加.细胞外K+浓度升高及应用TEA等均可使异位自发放电数升高.钙依赖性钾通道特异性阻断剂Apamin可显著增加其放电数.结论:改变DRG神经元的Ca(2+)浓度显著影响异位自发放电的放电数,其作用可能是通过钙依赖性钾通道的激活或抑制所致.
Aim: To elucidate the producing mechanism ofectopic spontaneous discharge (ESD) in neurons. Methods:Single dorsal root fibre was separated, the ESD conductedfrom injured dorsal root ganglion (DRG) neurons wasrecorded and the effects of the concentration of K+ and Ca2+and channel blockers were observed. Results: During[Ca2+]. had been enchanced or caffeine used, the number ofESD were inhibited while using Ni2+ or EGTA it werefacilitated. The increment of [K+]. and TEA could bothfacilitate the ESD. Apamin, a specific antagonist of calciumdependent potossium channel K (Ca), had markedly increasingeffect on ESD. Conclusion: The change of [Ca2+] can effectthe number of ESD from injured DRG neurons, whichmaybe act through the activation or inactivation of K(Ca).
出处
《第四军医大学学报》
1998年第6期614-617,共4页
Journal of the Fourth Military Medical University
基金
国家自然科学基金!39670247
关键词
背根神经节
异位自发放电
钙依赖性钾道
神经元
dorsal root ganglion ectopic spontaneous discharge calcium dependent potassium channel