Worley J F, McIntyre M S, Spencer B, Dukes I D
Department of Cell Physiology, Glaxo Research Institute, Research Triangle Park, North Carolina 27709.
J Biol Chem. 1994 Dec 23;269(51):32055-8.
Glucose stimulation of beta-cell insulin secretion is initiated by membrane depolarization coupled with an elevation in intracellular Ca2+ concentration ([Ca2+]i). Both depolarization-dependent Ca2+ entry and intracellular Ca2+ store release contribute to the sugar-induced rise in [Ca2+]i. Here we show that maneuvers depleting intracellular Ca2+ stores induce membrane depolarization and a sustained nitrendipine-sensitive Ca2+ influx, whereas interventions promoting Ca2+ store refilling produce a hyperpolarization and inhibit Ca2+ influx. Both intracellular Ca2+ store depletion and maitotoxin activated a depolarizing nonselective cation current carried principally by Na+ in the physiological range of membrane potentials. The activation of such a current may form the paradigm by which excitable cells refill depleted intracellular Ca2+ stores by depolarization-driven opening of voltage-activated Ca2+ channels.
β细胞胰岛素分泌的葡萄糖刺激是由膜去极化与细胞内Ca2+浓度（[Ca2+]i）升高共同启动的。去极化依赖性Ca2+内流和细胞内Ca2+储存释放都有助于糖诱导的[Ca2+]i升高。在这里，我们表明，耗尽细胞内Ca2+储存的操作会诱导膜去极化和持续的尼群地平敏感的Ca2+内流，而促进Ca2+储存重新填充的干预措施会产生超极化并抑制Ca2+内流。细胞内Ca2+储存耗尽和 maitotoxin 均激活了一种去极化的非选择性阳离子电流，该电流在膜电位的生理范围内主要由 Na+ 携带。这种电流的激活可能形成了一种模式，通过这种模式，可兴奋细胞通过去极化驱动的电压激活Ca²⁺通道开放来重新填充耗尽的细胞内Ca²⁺储存。
