Oliver Dominik, Lien Cheng-Chang, Soom Malle, Baukrowitz Thomas, Jonas Peter, Fakler Bernd
Institute of Physiology, University of Freiburg, Hermann-Herder-Strabetae 7, 79104 Freiburg, Germany.
Science. 2004 Apr 9;304(5668):265-70. doi: 10.1126/science.1094113. Epub 2004 Mar 18.
Voltage-gated potassium (Kv) channels control action potential repolarization, interspike membrane potential, and action potential frequency in excitable cells. It is thought that the combinatorial association between distinct alpha and beta subunits determines whether Kv channels function as non-inactivating delayed rectifiers or as rapidly inactivating A-type channels. We show that membrane lipids can convert A-type channels into delayed rectifiers and vice versa. Phosphoinositides remove N-type inactivation from A-type channels by immobilizing the inactivation domains. Conversely, arachidonic acid and its amide anandamide endow delayed rectifiers with rapid voltage-dependent inactivation. The bidirectional control of Kv channel gating by lipids may provide a mechanism for the dynamic regulation of electrical signaling in the nervous system.
电压门控钾（Kv）通道控制可兴奋细胞的动作电位复极化、峰间膜电位和动作电位频率。人们认为，不同的α和β亚基之间的组合关联决定了Kv通道是作为非失活延迟整流器还是快速失活A型通道发挥作用。我们发现，膜脂可以将A型通道转变为延迟整流器，反之亦然。磷酸肌醇通过固定失活结构域，消除A型通道的N型失活。相反，花生四烯酸及其酰胺类物质花生四烯酸乙醇胺赋予延迟整流器快速电压依赖性失活特性。脂质对Kv通道门控的双向控制可能为神经系统电信号的动态调节提供一种机制。
