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出 处:《生理学报》1997年第1期45-53,共9页Acta Physiologica Sinica
基 金:上海生命科学联合开放研究实验室资助!932105
摘 要:本工作用全细胞膜片箝记录的方法,观察了氟哌啶醇(haloperidol,以下简称HALO)和R(-)-Propyinoramorphine(以下简称NPA)对C6神经胶质瘤细胞(C6gliomacells)的电压依赖性钾电流的作用,并初步分析了它们的作用机制。结果表明,HALO和NPA都能抑制C6细胞的K+流,其抑制作用是可逆的,而且都与药物浓度有依赖关系。两者所抑制的主要是K+电流中的慢成分,而对快成分的作用有所不同。它们的抑制作用不是由多巴胺D2受体介导的,也不是通过G-蛋白或细胞内钙作用的,很可能是直接作用于钾通道。In this study, the inhibitory effects of R (-) - NPA (R (-) - Propylnorapomorphine) and haloperidol on voltage-dependent K+ currents in rat C6 glioma cells (C6 eells) were observed by means of the whole-cell patch-clamp recording technique.The mechanisms of the effects were aiso analyzed. The main results were as follows:(1) Both R (-) -NPA and haloperidol could inhibit K+ currents dose-dependently andreversibly in C6 cells. (2) R (-) -NPA and haloperidol inhibited mainly the slow component of the K+ currents. (3) These inhibitory respollas were not mediated bydopamine receptors or dependent on G-proteins and intracellular calcium. It was suggested they refer to some direct action on K+ channels.
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