Cook D L, Porte D, Crill W E
Am J Physiol. 1981 Mar;240(3):E290-6. doi: 10.1152/ajpendo.1981.240.3.E290.
The origin and control of glucose-induced rhythmic plateau potentials of pancreatic islet cells have been studied with intracellular microelectrodes in isolated mouse islets. Rapid changes of extracellular potassium concentration and direct electrical stimulation via a suction electrode were used to perturb islet cell membrane potentials. We show that brief depolarizing stimuli trigger permature plateau potentials, and brief hyperpolarizing currents abort endogenous plateaus. Both responses occur in an all-or-none manner, show a reciprocal relationship between stimulus strength and stimulus duration, have stimulus thresholds that approach zero at the time of the endogenous event, and completely reset the endogenous plateau rhythm. These results indicate that the plateau potentials are due to voltage-dependent regenerative mechanisms as in other electrically excitable tissues and implicate membrane potential or membrane ionic fluxes in the glucose-dependent pacemaker system that triggers their onset and offset.
利用细胞内微电极对分离的小鼠胰岛中葡萄糖诱导的胰岛细胞节律性平台电位的起源和控制进行了研究。通过改变细胞外钾离子浓度以及使用吸引导管电极进行直接电刺激来扰动胰岛细胞膜电位。我们发现,短暂的去极化刺激会触发早熟的平台电位,而短暂的超极化电流则会终止内源性平台电位。这两种反应均以全或无的方式发生,刺激强度与刺激持续时间之间呈反比关系,在内源性事件发生时刺激阈值接近零,并能完全重置内源性平台节律。这些结果表明,平台电位是由电压依赖性再生机制引起的,如同在其他电兴奋性组织中一样,并且表明膜电位或膜离子通量参与了触发其起始和终止的葡萄糖依赖性起搏器系统。