Depolarization and activation of dihydropyridine-sensitive Ca2+ channels stimulate inositol phosphate accumulation in photoreceptor-enriched chick retinal cell cultures.

Elevated concentrations of extracellular K+ increased inositol phosphate accumulation in primary cultures of chick retinal photoreceptors and multipolar neurons. K+-evoked stimulation of inositol phosphate accumulation was greater in photoreceptor-enriched cell cultures than in cultures where multipolar neurons were the predominant cell type. Destroying multipolar neurons, but not photoreceptors, with kainic acid and N-methyl-D-aspartate did not reduce the K+-evoked stimulation of inositol phosphate accumulation. Both of these observations indicate that the observed effects occur in photoreceptor cells. The K+-evoked stimulation of inositol phosphate accumulation was blocked by omitting Ca2+ from the incubation medium or by adding the dihydropyridine-sensitive Ca2+-channel antagonists, nitrendipine and nifedipine. Bay K 8644, a dihydropyridine agonist, stimulated inositol phosphate accumulation and enhanced the effect of K+. omega-Conotoxin GVIA, an inhibitor of N-type Ca2+ channels, had no significant effect on K+-stimulated inositol phosphate accumulation. Pretreatment with pertussis toxin neither blocked K+-evoked inositol phosphate accumulation nor altered the inhibitory effect of nifedipine. K+-evoked inositol phosphate accumulation appears to reflect activation of phosphatidylinositol-specific phospholipase C, as it is inhibited by U-73122. These results indicate that Ca2+ influx through voltage-gated, dihydropyridine-sensitive channels activates phospholipase C in photoreceptor inner segments and/or synaptic terminals.