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

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.