Bertram R, Smolen P, Sherman A, Mears D, Atwater I, Martin F, Soria B
Mathematical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Biophys J. 1995 Jun;68(6):2323-32. doi: 10.1016/S0006-3495(95)80414-5.
S. Bordin and colleagues have proposed that the depolarizing effects of acetylcholine and other muscarinic agonists on pancreatic beta-cells are mediated by a calcium release-activated current (CRAC). We support this hypothesis with additional data, and present a theoretical model which accounts for most known data on muscarinic effects. Additional phenomena, such as the biphasic responses of beta-cells to changes in glucose concentration and the depolarizing effects of the sarco-endoplasmic reticulum calcium ATPase pump poison thapsigargin, are also accounted for by our model. The ability of this single hypothesis, that CRAC is present in beta-cells, to explain so many phenomena motivates a more complete characterization of this current.
S. 博尔丁及其同事提出,乙酰胆碱和其他毒蕈碱激动剂对胰腺β细胞的去极化作用是由钙释放激活电流(CRAC)介导的。我们用更多数据支持这一假设,并提出一个理论模型,该模型解释了关于毒蕈碱效应的大多数已知数据。我们的模型还解释了其他现象,如β细胞对葡萄糖浓度变化的双相反应以及肌浆网钙ATP酶泵抑制剂毒胡萝卜素的去极化作用。CRAC存在于β细胞这一单一假设能够解释如此多现象,这促使我们对这种电流进行更全面的表征。