CAJ | 학술논문

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.
목적:탐토양감수과정삼여대갑통도조제적가설.방법:응용신선분리적소서배근신경절소세포,채용전세포막편겸기록IK전류.결과:당소세포결양시,갑통도재3 min지내즉가발생변화,표현위절대다수(86%, 6/7)세포적IK감약,1개세포(14%,1/7)적IK전류증강;결양1 min시IK감약,3 min시산생최대억제.당측시전위종+10 mV지+70 mV시,급성결양현저성강저IK,IK전류밀도강저최대폭도종(304.4±122.9)강위(253.9±106.4)pA·pF-1,단IK은태격활곡선무명현변화.결론:급성결양억제소서배근신경절소세포IK전류,이IK전류적억제작용가능시외주신경세포대결양적일충괄응화보호궤제.
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.