Grissmer S, Cahalan M
Department of Physiology and Biophysics, University of California, Irvine 92717.
Biophys J. 1989 Jan;55(1):203-6. doi: 10.1016/S0006-3495(89)82793-6.
The whole-cell recording mode of the patch-clamp technique was used to study the effect of external tetraethylammonium ([TEA+]o) on the inactivating, voltage-dependent K+ channels of human T lymphocytes. TEA+ reduced the peak amplitude and slowed the time course of the K+ current decay during a depolarizing pulse, resulting in a crossover of the current records in the presence and absence of TEA+. In solutions with different [TEA+]o both the peak K+ current amplitude, lKpeak, and the time constant of the decay of the K+ current, tau d, were reduced in a dose-dependent manner, both with apparent binding constants, KD, of 12 mM. The integral of K+ current during a prolonged depolarizing pulse was unaltered in solutions with different [TEA+]o. The concentration dependence of [TEA+]o on lKpeak, tau d, and the unchanged current integral can be explained with a kinetic scheme in which open channels blocked by TEA+ cannot inactivate.
采用膜片钳技术的全细胞记录模式,研究细胞外四乙铵([TEA+]o)对人T淋巴细胞中失活的、电压依赖性钾通道的影响。在去极化脉冲期间,TEA+降低了钾电流的峰值幅度,并减缓了钾电流衰减的时间进程,导致有无TEA+时的电流记录出现交叉。在不同[TEA+]o的溶液中,钾电流峰值幅度lKpeak和钾电流衰减时间常数tau d均呈剂量依赖性降低,表观结合常数KD均为12 mM。在不同[TEA+]o的溶液中,长时间去极化脉冲期间钾电流的积分未发生改变。[TEA+]o对lKpeak、tau d以及不变的电流积分的浓度依赖性可用一个动力学模型来解释,即被TEA+阻断的开放通道不能失活。