Journal
PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY
Volume 107, Issue 2, Pages 224-235Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbiomolbio.2011.06.009
Keywords
Pancreas; Beta-cell; Insulin; Ion channels; Glucose; Electrical activity
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Funding
- Wellcome Trust
- British MRC
- Diabetes UK
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When exposed to intermediate glucose concentrations (6-16 mol/l), pancreatic beta-cells in intact islets generate bursts of action potentials (superimposed on depolarised plateaux) separated by repolarised electrically silent intervals. First described more than 40 years ago, these oscillations have continued to intrigue beta-cell electrophysiologists. To date, most studies of beta-cell ion channels have been performed on isolated cells maintained in tissue culture (that do not burst). Here we will review the electrophysiological properties of beta-cells in intact, freshly isolated, mouse pancreatic islets. We will consider the role of ATP-regulated K(+)-channels (K(ATP)-channels), small-conductance Ca(2+)-activated K(+)-channels and voltage-gated Ca(2+)-channels in the generation of the bursts. Our data indicate that K(ATP)-channels not only constitute the glucose-regulated resting conductance in the beta-cell but also provide a variable K(+)- conductance that influence the duration of the bursts of action potentials and the silent intervals. We show that inactivation of the voltage-gated Ca(2+)-current is negligible at voltages corresponding to the plateau potential and consequently unlikely to play a major role in the termination of the burst. Finally, we propose a model for glucose-induced beta-cell electrical activity based on observations made in intact pancreatic islets. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved.
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