Chen W, Lee R C
Department of Surgery, University of Chicago, Illinois 60637.
Biophys J. 1994 Aug;67(2):603-12. doi: 10.1016/S0006-3495(94)80520-X.
The effects of large magnitude transmembrane potential pulses on voltage-gated Na and K channel behavior in frog skeletal muscle membrane were studied using a modified double vaseline-gap voltage clamp. The effects of electroconformational damage to ionic channels were separated from damage to lipid bilayer (electroporation). A 4 ms transmembrane potential pulse of -600 mV resulted in a reduction of both Na and K channel conductivities. The supraphysiologic pulses also reduced ionic selectivity of the K channels against Na+ ions, resulting in a depolarization of the membrane resting potential. However, TTX and TEA binding effects were unaltered. The kinetics of spontaneous reversal of the electroconformational damage of channel proteins was found to be dependent on the magnitude of imposed membrane potential pulse. These results suggest that muscle and nerve dysfunction after electrical shock may be in part caused by electroconformational damage to voltage-gated ion channels.
使用改良的双凡士林间隙电压钳研究了大幅度跨膜电位脉冲对蛙骨骼肌膜电压门控钠通道和钾通道行为的影响。将离子通道的电构象损伤效应与脂质双层损伤(电穿孔)区分开来。-600 mV的4 ms跨膜电位脉冲导致钠通道和钾通道电导率均降低。超生理脉冲还降低了钾通道对钠离子的离子选择性,导致膜静息电位去极化。然而,TTX和TEA结合效应未改变。发现通道蛋白电构象损伤的自发逆转动力学取决于施加的膜电位脉冲幅度。这些结果表明,电击后肌肉和神经功能障碍可能部分是由电压门控离子通道的电构象损伤引起的。