DEPOLARIZATION AND ACTIVATION OF DIHYDROPYRIDINE-SENSITIVE CA2-ENRICHED CHICK RETINAL CELL-CULTURES( CHANNELS STIMULATE INOSITOL PHOSPHATE ACCUMULATION IN PHOTORECEPTOR)

Elevated concentrations of extracellular K+ increased inositol phospha te accumulation in primary cultures of chick retinal photoreceptors an d multipolar neurons. K+-evoked stimulation of inositol phosphate accu mulation was greater in photoreceptor-enriched cell cultures than in c ultures where multipolar neurons were the predominant cell type. Destr oying multipolar neurons, but not photoreceptors, with kainic acid and N-methyl-D-aspartate did not reduce the K+-evoked stimulation of inos itol phosphate accumulation. Both of these observations indicate that the observed effects occur in photoreceptor cells. The K+-evoked stimu lation 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 an d enhanced the effect of K+. omega-Conotoxin GVIA, an inhibitor of N-t ype Ca2+ channels, had no significant effect on K+-stimulated inositol phosphate accumulation. Pretreatment with pertussis toxin neither blo cked K+-evoked inositol phosphate accumulation nor altered the inhibit ory effect of nifedipine. K+-evoked inositol phosphate accumulation ap pears to reflect activation of phosphatidylinositol-specific phospholi pase C, as ii is inhibited by U-73122. These results indicate that Ca2 + influx through voltage-gated, dihydropyridine-sensitive channels act ivates phospholipase C in photoreceptor inner segments and/or synaptic terminals.