Bursting electrical activity in pancreatic beta cells caused by Ca(2+)- and voltage-inactivated Ca2+ channels.
We investigate the hypothesis that two classes of Ca2+ currents, one quickly inactivated by Ca2+ and one slowly inactivated by voltage, contribute to bursting electrical activity in pancreatic islets. A mathematical model of these currents is fit to the experimental whole-cell current-voltage and inactivation profiles, thereby fixing the Ca2+ conductance and all activation and inactivation parameters. Incorporating these currents into a model that includes delayed rectifier K+ channels and ATP-sensitive K+ channels, we show that only abnormal bursting is obtained. Modification of activation parameters to increase Ca2+ channel open times, as suggested by experiment, yields a more robust bursting similar to that observed in intact islets. This reinforces the suggestion that in addition to ATP-sensitive K+ channels, Ca2+ channels may serve as glucose sensors in the beta cell.
Keizer
J
J
Institute of Theoretical Dynamics, University of California, Davis 95616.
Smolen
P
P
D002118:Calcium / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology*; D004553:Electric Conductivity; D004594:Electrophysiology; D007515:Islets of Langerhans / Q000502:physiology*; D008564:Membrane Potentials; D008962:Models, Theoretical; D011188:Potassium / Q000502:physiology
D015220:Calcium Channels; D011188:Potassium; D002118:Calcium