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

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.

• Author: Sven Göpel; Takahiro Kanno; Sebastian Barg; Lena Eliasson; Juris Galvanovskis; Erik Renström; Patrik Rorsman
• 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
• Links: http://www.jgp.org/cgi/content/full/114/6/759
• 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