BmKAS-1和BmK1-3-2对大鼠背根神经节神经元钠电流的影响
Modulation of BmKAS-1 and BmK1-3-2 to sodium channel in rat dorsal root ganglion neurons
目的 研究新的蝎毒素纯化多肽BmKAS-1及其前级提取物BmK1-3-2对大鼠背根神经节小直径神经元钠通道电流的作用,并探讨两者与其外周镇痛作用间的关系。 方法 运用全细胞膜片箝技术观察了BmKAS-1和BmK1-3-2对钠电流的作用。 结果 10μg/ml的BmK1-3-2可阻断约50%的峰钠电流,而1.62μg/ml 的BmKAS-1即可达到相同的阻断效果,同时BmKAS-1对钠电流的作用呈现出明显的剂量反应关系。 结论 BmKAS-1和BmK1-3-2对钠电流均有较强的抑制作用。鉴于钠通道与损伤所致的外周神经元感觉过敏有关,这种抑制作用可能是BmKAS-1和BmK1-3-2外周镇痛作用的机制之一。
更多Objective To investigate what effects BmKAS-1 (a polypeptide purified from the Chinese scorpion Buthus martensi Karsch [BmK] and named as BmK activator of skeletal-muscle ryanodine receptor) and its upstream mixture BmK1-3-2 have on Na+ channels in dorsal root ganglion (DRG) small diameter neurons.Methods The whole-cell patch-clamp technique was used to investigate the effects of BmKAS-1 and BmK1-3-2 on Na+ current in rat small diameter DRG neurons.Results About 50% peak Na+ current was suppressed by 10*!μg/ml of BmK1-3-2. 1.62*!μg/ml of BmKAS-1 also blocked 50% peak Na+ current, and there was an obvious dose-dependent relationship.Conclusion Both BmK1-3-2 and BmKAS-1 have a blocking effect on Na+ channels, and this may one of the mechanisms for the analgetic effect of BmK1-3-2 and BmKAS-1.
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