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J Physiol Volume 545, Number 2, 501-507, December 1, 2002 DOI: 10.1113/jphysiol.2002.031344
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Journal of Physiology (2002), 545.2, pp. 501-507
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2002.031344

Glucose-dependent regulation of rhythmic action potential firing in pancreatic beta-cells by KATP-channel modulation

T. Kanno, P. Rorsman * and S. O. Göpel *

Department of Physiology, Hirosaki University School of Medicine, Japan and * Institute of Physiological Sciences, Department of Molecular and Cellular Physiology, Lund University, Sweden

The regulation of a K+ current activating during oscillatory electrical activity (IK,slow) in an insulin-releasing beta-cell was studied by applying the perforated patch whole-cell technique to intact mouse pancreatic islets. The resting whole-cell conductance in the presence of 10 mM glucose amounted to 1.3 nS, which rose by 50 % during a series of 26 simulated action potentials. Application of the KATP-channel blocker tolbutamide produced uninterrupted action potential firing and reduced IK,slow by ~50 %. Increasing glucose from 15 to 30 mM, which likewise converted oscillatory electrical activity into continuous action potential firing, reduced IK,slow by ~30 % whilst not affecting the resting conductance. Action potential firing may culminate in opening of KATP channels by activation of ATP-dependent Ca2+ pumping as suggested by the observation that the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor thapsigargin (4 µM) inhibited IK,slow by 25 % and abolished bursting electrical activity. We conclude that oscillatory glucose-induced electrical activity in the beta-cell involves the opening of KATP-channel activity and that these channels, in addition to constituting the glucose-regulated K+ conductance, also play a role in the graded response to supra-threshold glucose concentrations.



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