【摘要】 目的:探讨氧感受过程参与对钾通道调制的假设。方法:应用新鲜分离的小鼠背根神经节小细胞,采用全细胞膜片钳记录IK电流。结果:当小细胞缺氧时,钾通道在3 min之内即可发生变化,表现为绝大多数(86%,6/7)细胞的IK减弱,1个细胞(14%,1/7)的IK电流增强;缺氧1 min时IK减弱,3 min时产生最大抑制。当测试电位从+10 mV至+70 mV时,急性缺氧显著性降低IK,IK电流密度降低最大幅度从(304.4±122.9)降为(253.9±106.4)pA.pF-1,但IK稳态激活曲线无明显变化。结论:急性缺氧抑制小鼠背根神经节小细胞IK电流,而IK电流的抑制作用可能是外周神经细胞对缺氧的一种适应和保护机制。更多还原

【Abstract】 Objective Modulation of K+ channel had been shown to be an integral and important cellular response to O2 deprivation.Method Freshly dissociated neurons from mouse dorsal root ganglion(DRG) were used to test the hypothesis that O2-sensing process was involved in the modulation of K+ channel activity.Whole-cell patch clamp technique was used to record the change in IK of K+ channel.Results Hypoxia caused the change in IK in small size DRG neurons.They responded within 3 min with a change in IK.Majority of cells displayed a reduction in IK during the time course of patch clamp experiment,whereas one out of seven neurons showed an increase in IK.IK inhibition started about 1 min after the onset of hypoxia and maximum inhibition was reached in about 3 min.Hypoxia decreased the IK from test potential of 10 to 70 mV and the utmost decrease was from(304.4±122.9) to(253.9±106.4) pA·pF-1,whereas steady-state activation of IK was not changed significantly.Conclusion The study indicates that hypoxia induced an inhibition of IK in small size DRG neurons and this inhibition of IK might play a protective action in adapting to O2 deprivation in acute and short-term hypoxia.更多还原