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

Författare

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.

Publiceringsår

1999

Språk

Engelska

Sidor

759-770

Publikation/Tidskrift/Serie

Journal of General Physiology

Volym

114

Issue

6

Dokumenttyp

Artikel i tidskrift

Förlag

Rockefeller Institute for Medical Research

Ämne

  • Endocrinology and Diabetes

Nyckelord

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

Status

Published

Forskningsgrupp

  • Islet cell physiology

ISBN/ISSN/Övrigt

  • ISSN: 0022-1295