Cyclic variation of K+ conductance in pancreatic beta-cells: Ca2+ and voltage dependence.

Pulses of hyperpolarizing current were injected through the microelectrode recording the electrical activity of beta-cells in order to measure input resistance. Increase in resistance during depolarization of the slow oscillation ("burst") indicates inactivation of an outward current, probably K+. Decrease in resistance as the plateau commences suggests that the previous depolarization causes activation of an inward current, probably calcium. The postburst hyperpolarization, caused by a late activation of potassium permeability (PK), would result from the increase of intracellular free calcium. An intracellular buffering system may control this intracellular free calcium level. By restoring the silent phases, in the presence of ouabain or high potassium, injection of hyperpolarizing current shows also a voltage dependency of the PK involved in the postburst hyperpolarization. Glucose, by stimulating intracellular binding of calcium, would cause membrane depolarization at glucose levels below threshold and elongation of the plateau phase at higher concentrations.