K+-EVOKED DEPOLARIZATION STIMULATES CYCLIC-AMP ACCUMULATION IN PHOTORECEPTOR-ENRICHED RETINAL CELL-CULTURES - ROLE OF CALCIUM INFLUX THROUGH DIHYDROPYRIDINE-SENSITIVE CALCIUM CHANNELS

The effect of membrane depolarization on cyclic AMP synthesis was studied in glia-free, low-density, monolayer cultures of chick retinal photoreceptors and neurons. In photoreceptor-enriched cultures prepared from embryonic day 6 retinas and cultured for 6 days, elevated K+ concentrations increased the intracellular concentration of cyclic AMP and stimulated the conversion of [H-3]adenine to [H-3]cyclic AMP. The K+-evoked increase of cyclic AMP accumulation was blocked by omitting CaCl2 from the incubation medium, indicating a requirement for extracellular Ca2+. Stimulation of cyclic AMP accumulation was also inhibited by nifedipine, methoxyverapamil, Cd2+, Co2+, and Mg2+, and was enhanced by the dihydropyridine Ca2+ channel agonist Bay K 8644. The enhancement of K+-evoked cyclic AMP accumulation by Bay K 8644 was antagonized by nifedipine. Thus, Ca2+ influx through dihydropyridine-sensitive channels is required for depolarization-evoked stimulation of cyclic AMP accumulation in photoreceptor-enriched cultures.