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Erik Renström

Erik Renström

Vice-chancellor

Erik Renström

Activation of Ca(2+)-dependent K(+) channels contributes to rhythmic firing of action potentials in mouse pancreatic beta cells

Author

  • Sven Göpel
  • Takahiro Kanno
  • Sebastian Barg
  • Lena Eliasson
  • Juris Galvanovskis
  • Erik Renström
  • Patrik Rorsman

Summary, in English

We have applied the perforated patch whole-cell technique to beta cells within intact pancreatic islets to identify the current underlying the glucose-induced rhythmic firing of action potentials. Trains of depolarizations (to simulate glucose-induced electrical activity) resulted in the gradual (time constant: 2.3 s) development of a small (<0.8 nS) K(+) conductance. The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) channels, and was insensitive to tolbutamide (a blocker of ATP-regulated K(+) channels) but partially (>60%) blocked by high (10-20 mM) concentrations of tetraethylammonium. Upon cessation of electrical stimulation, the current deactivated exponentially with a time constant of 6.5 s. This is similar to the interval between two successive bursts of action potentials. We propose that this Ca(2+)-activated K(+) current plays an important role in the generation of oscillatory electrical activity in the beta cell.

Department/s

  • Department of Experimental Medical Science
  • Islet cell physiology
  • Department of Clinical Sciences, Malmö

Publishing year

1999

Language

English

Pages

759-770

Publication/Series

Journal of General Physiology

Volume

114

Issue

6

Document type

Journal article

Publisher

Rockefeller Institute for Medical Research

Topic

  • Endocrinology and Diabetes

Keywords

  • Ca2+-activated K+ channel
  • pancreas
  • insulin
  • Ca2+
  • membrane potential

Status

Published

Research group

  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 0022-1295