title: Electrical pacemaker mechanisms of pancreatic islet cells.
abstract: Glucose, the major physiological stimulus for insulin secretion, induces a periodic bursting pattern of Ca2+ action potentials that are thought to mediate the uptake of Ca2+ into the intracellular pool of free Ca2+, which controls the rate of insulin release. Evidence is reviewed that shows that the voltage-dependent Ca2+ spikes are driven by a slow, voltage-dependent plateau depolarization that may also be caused by Ca2+ influx. Current evidence suggests that this plateau conductance is periodically terminated in turn by a pacemaker current through membrane K+ channels that are activated by intracellular free Ca2+. The control of electrical activity by different modulators of insulin release may involve interactions with this system at several points, including changes of the sensitivity of K+ channels to intracellular Ca2+ and to changes of intracellular Ca2+ buffering capacity.
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology; D004553:Electric Conductivity; D004594:Electrophysiology; D004837:Epinephrine / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007473:Ion Channels / Q000502:physiology; D007515:Islets of Langerhans / Q000502:physiology*; D011188:Potassium / Q000502:physiology
chemical_list: D007328:Insulin; D007473:Ion Channels; D005947:Glucose; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium; D004837:Epinephrine