Activation of Ca<sup>2+</sup>-dependent K<sup>+</sup>channels contributes to rhythmic firing of action potentials in mouse pancreatic β cells
Göpel SO., Kanno T., Barg S., Eliasson L., Galvanovskis J., Renström E., Rorsman P.
We have applied the perforated patch whole-cell technique to 13 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.