K+-EVOKED DEPOLARIZATION INDUCES SEROTONIN N-ACETYLTRANSFERASE ACTIVITY IN PHOTORECEPTOR-ENRICHED RETINAL CELL-CULTURES - INVOLVEMENT OF CALCIUM INFLUX THROUGH L-TYPE CHANNELS

The roles of membrane depolarization and calcium influx in the regulation of retinal serotonin N-acetyltransferase (NAT) activity were investigated in low-density monolayer cultures of chick retinal cells, in which photoreceptors represented approximately 70% of the total cell population. NAT activity expressed by the cells in these cultures was markedly increased by elevating the concentration of extracellular K+. Activity increased rapidly during the first 6 h of exposure to K+, and remained elevated for at least 30 h. Chelation of calcium in the culture medium abolished the K+-evoked increase in NAT activity. Antagonists of voltage-sensitive calcium channels, nifedipine, methoxyverapamil (D600), Mn2+, Mg2+, and Cd2+ inhibited the K+-evoked increase of NAT activity. Bay K 8644, a dihydropyridine calcium channel agonist, increased NAT activity when added alone and potentiated the K+-evoked increase of activity. The effect of Bay K 8644 was antagonized by nifedipine. Addition of nifedipine 18 h after addition of K+, when NAT activity is elevated, caused activity to decrease to basal levels. These studies indicate that the increase of retinal NAT activity induced by K+-depolarization is mediated by a calcium-dependent process that involves sustained Ca2+ influx through L-type voltage-sensitive Ca2+-channels. © 1990.