Fakler B, Brändle U, Glowatzki E, Weidemann S, Zenner H P, Ruppersberg J P
Department of Sensory Biophysics, Hospital of the University of Tübingen, Federal Republic of Germany.
Cell. 1995 Jan 13;80(1):149-54. doi: 10.1016/0092-8674(95)90459-x.
Inward rectifier K+ channels mediate the K+ conductance at resting potential in many types of cell. Since these K+ channels do not pass outward currents (inward rectification) when the cell membrane is depolarized beyond a trigger threshold, they play an important role in controlling excitability. Both a highly voltage-dependent block by intracellular Mg2+ and an endogenous gating process are presently assumed to underly inward rectification. It is shown that strong voltage dependence of rectification found under physiological conditions is predominantly due to the effect of intracellular spermine. Physiological concentrations of free spermine mediate strong rectification of IRK1 inward rectifier K+ channels even in the absence of free Mg2+ and in IRK1 mutant channels that have no endogenous rectification.
内向整流钾通道介导多种细胞静息电位时的钾离子电导。由于当细胞膜去极化超过触发阈值时，这些钾通道不通过外向电流（内向整流），它们在控制兴奋性方面发挥重要作用。目前认为，内向整流主要由细胞内镁离子的高度电压依赖性阻滞和内源性门控过程引起。研究表明，生理条件下发现的整流的强电压依赖性主要归因于细胞内精胺的作用。即使在没有游离镁离子的情况下，以及在没有内源性整流的IRK1突变通道中，生理浓度的游离精胺也能介导IRK1内向整流钾通道的强整流作用。
