The regulation of a K+ current activating during oscillatory electrical activity (IK,slow) in an insulin-releasing β-cell was studied by applying the perforated patch whole-cell technique to intact mouse pancreatic islets. The resting whole-cell conductance in the presence of 10 mm glucose amounted to 1.3 nS, which rose by 50 % during a series of 26 simulated action potentials. Application of the KATP-channel blocker tolbutamide produced uninterrupted action potential firing and reduced IK,slow by ≈50 %. Increasing glucose from 15 to 30 mm, which likewise converted oscillatory electrical activity into continuous action potential firing, reduced IK,slow by ≈30 % whilst not affecting the resting conductance. Action potential firing may culminate in opening of KATP channels by activation of ATP-dependent Ca2+ pumping as suggested by the observation that the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor thapsigargin (4 μm) inhibited IK,slow by 25 % and abolished bursting electrical activity. We conclude that oscillatory glucose-induced electrical activity in the β-cell involves the opening of KATP-channel activity and that these channels, in addition to constituting the glucose-regulated K+ conductance, also play a role in the graded response to supra-threshold glucose concentrations
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