Slow voltage inactivation of Ca2+ currents and bursting mechanisms for the mouse pancreatic beta-cell.
Recent whole-cell electrophysiological data concerning the properties of the Ca2+ currents in mouse beta-cells are fitted by a two-current model of Ca2+ channel kinetics. When the beta-cell K+ currents are added to this model, only large modifications of the measured Ca2+ currents will reproduce the bursting pattern normally observed in mouse islets. However, when the measured Ca2+ currents are modified only slightly and used in conjunction with a K+ conductance that can be modulated dynamically by ATP concentration, reasonable bursting is obtained. Under these conditions it is the K-ATP conductance, rather than the slow voltage inactivation of the Ca2+ current, that determines the interburst interval. We find that this latter model can be reconciled with experiments that limit the possible periodic variation of the K-ATP conductance and with recent observations of intracellular Ca2+ bursting in islets.
Smolen
P
P
National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892.
Keizer
J
J
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism*; D004594:Electrophysiology; D007515:Islets of Langerhans / Q000378:metabolism* / Q000502:physiology; D007700:Kinetics; D051379:Mice; D008954:Models, Biological
D015220:Calcium Channels; D002118:Calcium