The Journal of General Physiology
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Published online 1 December 1999.
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© The Rockefeller University Press, 0022-1295/1999//759/ $5.00
Journal of General Physiology, Volume 114, Number 6, 1999

Original Article

Activation of Ca2+-Dependent K+ Channels Contributes to Rhythmic Firing of Action Potentials in Mouse Pancreatic β Cells

Sven O. Göpela, Takahiro Kannoa, Sebastian Barga, Lena Eliassona, Juris Galvanovskisa, Erik Renströma, and Patrik Rorsmana

a From the Department of Physiological Sciences, Division of Molecular and Cellular Physiology, Lund University, SE-223 62 Lund, Sweden
Department of Physiological Sciences, Division of Molecular and Cellular Physiology, Lund University, Sölvegatan 19, SE-223 62 Lund, Sweden.46-46-222 77 63

patrik.rorsman{at}mphy.lu.se

We have applied the perforated patch whole-cell technique to β 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 Ca2+ influx but unaffected by apamin and charybdotoxin, two blockers of Ca2+-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 Ca2+-activated K+ current plays an important role in the generation of oscillatory electrical activity in the β cell.

Key Words: insulin • pancreas • Ca2+-activated K+ channel • Ca2+ • membrane potential

© 1999 The Rockefeller University Press


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