Potassium and chloride currents in rat gastric enterochromaffin-like cells

¹ Department of Physiology, University of California at Los Angeles School of Medicine, Center for the Health Sciences, Los Angeles 90095-1751; and Digestive Disease Center, Center for Ulcer Research and Education, Department of Veterans Affairs, West Los Angeles Medical Center, Los Angeles, California 90073

The gastric enterochromaffin-like (ECL) cell se cretes histamine in response to secretagogues (gastrin, acetylcholine) by calcium signaling-dependent exocytosis of intracellular vacuoles containing the hormone. ECL cells were isolated from rat fundic gastric mucosa by elutriation and density-gradient centrifugation. Currents across the plasma membrane were measured using whole cell patch-clamp methods. These cells had a low conductance of 0.5 nS and resting potential of –50 mV Depolarization activated a K⁺ current that was blocked by Ba²⁺. Steady-state current in absence of K⁺ was due to Cl^– because of the magnitude of the reversal potential and the effects of Cl^– removal. Stimulation of secretion by gastrin, cholecystokinin octapeptide (CCK-8), and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate activated the Cl^– conductance with a time course similar to that of histamine release. Therefore the ECL cell maintains a high resting potential, largely due to K⁺ currents, and stimulation of secretion activates a Cl^– current, perhaps deriving from the membrane of the secretory granule that fuses with the plasma membrane. The depolarization that ensues may activate the K⁺ current to maintain the membrane potential during exocytosis.

exocytosis; acid secretion

Submitted on July 31, 1995
Accepted on October 2, 1995