Cook D L, Satin L S, Hopkins W F
Division of Metabolism, Seattle VA Medical Center, WA 98108.
Trends Neurosci. 1991 Sep;14(9):411-4. doi: 10.1016/0166-2236(91)90033-q.
Insulin secretogogues have long been known to stimulate and modulate bursting electrical activity in pancreatic islet B cells and thereby supply extracellular Ca2+ for the exocytosis of insulin. Recent results have ruled out a long-held hypothesis for the mechanism of burst formation that postulated key roles for intracellular Ca2+ accumulation and activation of Ca(2+)-activated K+ channels. Here, we present an alternative hypotheses based on a persistent Ca2+ conductance and, possibly, phasic activation of ATP-sensitive K+ channels. These hypotheses are compared with mechanisms of bursting proposed for invertebrate and mammalian neurons.
长期以来，人们都知道胰岛素促分泌剂能刺激并调节胰岛B细胞的爆发式电活动，从而为胰岛素的胞吐作用提供细胞外Ca2+。最近的研究结果排除了一个长期存在的关于爆发形成机制的假说，该假说假定细胞内Ca2+积累和Ca(2+)激活的K+通道的激活起关键作用。在此，我们提出了一种基于持续Ca2+电导以及可能的ATP敏感性K+通道阶段性激活的替代假说。这些假说与针对无脊椎动物和哺乳动物神经元提出的爆发机制进行了比较。
