Mouse pancreatic beta‐cells: tetraethylammonium blockage of the potassium permeability increase induced by depolarization.

Abstract

Membrane potentials and input resistance were measured in .beta.-cells from mouse pancreatic islets of Langerhans in the presence or absence of D-glucose. Tetraethylammonium (TEA) (a specific blocker of the K permeability increase induced by shifts in membrane potential from negative to positive values) was externally applied and its effects on potentials and input resistance evaluated. In the absence of glucose, addition of TEA up to 20 mM to the perfusion medium did not affect the resting potential and the input resistance, the selectivity ratio PK/PNa (calculated from the constant field equation) remaining unchanged at about 30. The characteristic response of the .beta.-cell membrane potential, in the presence of glucose, was a fluctuation between a silent phase at about -50 mV and an active phase at about -40 mV giving rise to a train of spikes. TEA abolished this pattern and very much reduced the graded response of spike frequency normally seen with different concentrations of glucose. Addition of glucose in the presence of up to 20 mM-TEA induced an increase in membrane resistance of about 4.107 .OMEGA.. TEA lowered the glucose level required to trigger the electrical activity from about 5.6-4.6 mM. TEA blocked the repolarization phase of action potentials induced by the addition of glucose or by depolarizing intracellular current injection. In the presence of 11.1 mM-glucose and 20 mM-TEA the action potentials frequently crossed the zero line, the membrane potential reaching up to 25 mV during the peak of the spikes.