Ribalet B, Beigelman P M
Am J Physiol. 1979 Sep;237(3):C137-46. doi: 10.1152/ajpcell.1979.237.3.C137.
Pulses of hyperpolarizing current were injected through the microelectrode recording the electrical activity of beta-cells in order to measure input resistance. Increase in resistance during depolarization of the slow oscillation ("burst") indicates inactivation of an outward current, probably K+. Decrease in resistance as the plateau commences suggests that the previous depolarization causes activation of an inward current, probably calcium. The postburst hyperpolarization, caused by a late activation of potassium permeability (PK), would result from the increase of intracellular free calcium. An intracellular buffering system may control this intracellular free calcium level. By restoring the silent phases, in the presence of ouabain or high potassium, injection of hyperpolarizing current shows also a voltage dependency of the PK involved in the postburst hyperpolarization. Glucose, by stimulating intracellular binding of calcium, would cause membrane depolarization at glucose levels below threshold and elongation of the plateau phase at higher concentrations.
通过微电极注入超极化电流脉冲，记录β细胞的电活动，以测量输入电阻。慢振荡（“爆发”）去极化期间电阻增加表明外向电流（可能是K+）失活。平台期开始时电阻降低表明先前的去极化导致内向电流（可能是钙）激活。爆发后超极化由钾通透性（PK）的晚期激活引起，这是细胞内游离钙增加的结果。细胞内缓冲系统可能控制这种细胞内游离钙水平。在哇巴因或高钾存在的情况下，通过恢复静息期，注入超极化电流也显示出爆发后超极化中涉及的PK的电压依赖性。葡萄糖通过刺激细胞内钙结合，在低于阈值的葡萄糖水平时会引起膜去极化，在较高浓度时会延长平台期。
