CALCIUM-DEPENDENT REGULATION OF CHOLECYSTOKININ SECRETION AND POTASSIUM CURRENTS IN STC-1 CELLS

Secretory and electrophysiological properties of STC-1 cells, a cholec ystokinin-secreting cell line, were examined with a radioimmunoassay a nd patch-clamp recording techniques. Stimulation of cholecystokinin se cretion was seen after exposure to agents anticipated to increase the level of intracellular calcium, including thapsigargin (8 muM), bombes in (50 nM), potassium-induced depolarization (50 mM), or after blockad e of potassium channels with barium chloride (2 mM). The secretory eff ects of these agents were blocked by pretreatment with the calcium cha nnel blocker diltiazem (1 muM). Whole cell patch-clamp recordings show ed a hyperpolarizing shift in reversal potential after exposure to eit her thapsigargin (8 muM) or bombesin (50 nM) from a control value of - 27 +/- 3 to -57 +/- 7 or -48 +/- 6 mV, respectively. This shift was in the direction of the reversal potential for potassium and was blocked by barium chloride (5 mM). Single-channel recordings from cell-attach ed membrane patches showed an inwardly rectifying potassium channel wi th channel open probability modulated by bombesin. These results indic ate that in STC-1 cells a potassium current is increased by agents tha t stimulate CCK secretion, presumably by increasing the level of cytos olic calcium. STC-1 cells may serve as a model system to study the ele ctrophysiological and secretory mechanisms involved in the release of cholecystokinin.