Regulation of melatonin synthesis in rainbow trout (Oncorhyncus mykiss) pineal organs: effects of calcium depletion and calcium channel drugs.

The effects of calcium depletion and of three calcium channel drugs on melatonin synthesis in pineal organs of rainbow trout (Oncorhyncus mykiss) were examined. Dark-induced melatonin synthesis was inhibited by calcium depletion, by treatment with nitrendipine (NTR), an antagonist of the L-type voltage-sensitive calcium channel, and by treatment with omega-Conotoxin GVIA, an antagonist of the N-type voltage-sensitive calcium channel. Bay K 8644, an agonist of the L-type channel, had no significant effect on pineal melatonin synthesis. These data represent evidence that calcium entry into trout pineal photoreceptor cells through voltage-sensitive calcium channels is important in the maintenance of dark-induced melatonin synthesis and that light's inhibitory effect on melatonin synthesis may be mediated by closure of these channels. NTR-induced inhibition of dark-induced melatonin synthesis was abolished when dibutyryl cyclic AMP (db-cAMP) was administered to NTR-treated pineal organs, suggesting that calcium acts upstream of cAMP in regulating melatonin synthesis.