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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
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

Abstract 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.

Keywords

  • Endocrinology and Diabetes
  • Ca2+-activated K+ channel
  • pancreas
  • insulin
  • Ca2+
  • membrane potential

Other

Published
  • Islet cell physiology
  • ISSN: 0022-1295
Erik Renström
E-mail: erik.renstrom [at] med.lu.se

Deputy head of department

Department of Clinical Sciences, Malmö

+46 40 39 11 57

+46 40 39 11 57

Principal investigator

Islet patophysiology

+46 40 39 11 57

+46 40 39 11 57

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