AJP - Cell Physiology, Vol 237, Issue 3 137-C146, Copyright © 1979 by American Physiological Society
Cyclic variation of K+ conductance in pancreatic beta-cells: Ca2+ and voltage dependence
B. Ribalet and P. M. Beigelman
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.
