title: Pancreatic B cells are bursting, but how?
abstract: 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.
authors.affiliation: Division of Metabolism, Seattle VA Medical Center, WA 98108.
authors.forename: D L
authors.initials: DL
authors.lastname: Cook
authors.forename: L S
authors.initials: LS
authors.lastname: Satin
authors.forename: W F
authors.initials: WF
authors.lastname: Hopkins
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology; D015220:Calcium Channels / Q000502:physiology; D004594:Electrophysiology; D006801:Humans; D007515:Islets of Langerhans / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology
chemical_list: D015220:Calcium Channels; D015221:Potassium Channels; D002118:Calcium