The typical burst pattern of electrical activity recorded from beta-cells of mouse islets in the presence of 11.1 mM glucose has been compared from 225 cells in terms of two parameters: relative duration of the active phase and periodicity of the oscillations between active and silent phases. The two parameters show different distributions, Gaussian and bimodal respectively. Burst periodicity was found to increase dramatically at external potassium concentrations below 2mM, while the relative duration of the active phase was little affected at concentrations as low as 0.5 mM. Increasing external calcium concentration significantly increased the amplitude of the bursts but greatly decreased the relative duration of the active phase. Quinine, in the absence of glucose, induced depolarization and electrical activity and stimulated insulin release from perifused mouse islets; spike frequency and insulin release followed a monophasic pattern. A model has been proposed for the beta-cell explaining the experimental results in terms of a feedback mechanism between calcium permeability activated by depolarization of the cell membrane and potassium permeability activated by an increase in the concentration of intracellular ionized calcium [Ca2+]i. The results are in agreement with the hypothesis that a [Ca2+]i-dependent potassium permeability, specifically blocked by quinine, controls membrane potential and insulin release.