A role for calcium release-activated current (CRAC) in cholinergic modulation of electrical activity in pancreatic beta-cells

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology
  • Animals
  • Calcium / metabolism*
  • Calcium-Transporting ATPases / antagonists & inhibitors
  • Carbachol / pharmacology
  • Cholinergic Agents / pharmacology*
  • Endoplasmic Reticulum / enzymology
  • Glucose / pharmacology
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / physiology*
  • Kinetics
  • Mathematics
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Mice
  • Models, Biological*
  • Sarcoplasmic Reticulum / enzymology
  • Terpenes / pharmacology
  • Thapsigargin
  • Time Factors


  • Cholinergic Agents
  • Insulin
  • Terpenes
  • Thapsigargin
  • Carbachol
  • Calcium-Transporting ATPases
  • Glucose
  • Acetylcholine
  • Calcium