Klemic K G, Shieh C C, Kirsch G E, Jones S W
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Biophys J. 1998 Apr;74(4):1779-89. doi: 10.1016/S0006-3495(98)77888-9.
We report here several unusual features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in Xenopus oocytes. The voltage dependence of inactivation was U-shaped, with maximum inactivation near 0 mV. During a maintained depolarization, development of inactivation was slow and only weakly voltage dependent (tau = 4 s at 0 mV; tau = 7 s at +80 mV). However, recovery from inactivation was strongly voltage dependent (e-fold for 20 mV) and could be rapid (tau = 0.27 s at -140 mV). Kv2.1 showed cumulative inactivation, where inactivation built up during a train of brief depolarizations. A single maintained depolarization produced more steady-state inactivation than a train of pulses, but there could actually be more inactivation with the repeated pulses during the first few seconds. We term this phenomenon "excessive cumulative inactivation." These results can be explained by an allosteric model, in which inactivation is favored by activation of voltage sensors, but the open state of the channel is resistant to inactivation.
我们在此报告了在非洲爪蟾卵母细胞中表达的大鼠Kv2.1延迟整流钾通道失活的几个不寻常特征。失活的电压依赖性呈U形，在接近0 mV时失活最大。在持续去极化期间，失活的发展缓慢且仅弱电压依赖性（在0 mV时τ = 4 s；在+80 mV时τ = 7 s）。然而，从失活中恢复强烈依赖电压（20 mV时为e倍）且可能很快（在-140 mV时τ = 0.27 s）。Kv2.1表现出累积失活，即在一系列短暂去极化期间失活逐渐累积。单次持续去极化产生的稳态失活比一系列脉冲更多，但在最初几秒内重复脉冲实际上可能导致更多失活。我们将此现象称为“过度累积失活”。这些结果可以用变构模型来解释，其中电压传感器的激活有利于失活，但通道的开放状态对失活具有抗性。
