Evidence against alpha2-adrenoceptor involvement in the regulation of rat melatonin synthesis by ambient lighting

This study was carried out to clarify the role of alpha(2)-adrenoceptors in the regulation of pineal melatonin synthesis. Medetomidine, a selective al pha(2)-adrenoceptor agonist, was previously found to be a potent suppressor of nocturnal melatonin levels in rats. Medetomidine and alpha(2)-adrenocep tor antagonists atipamezole and yohimbine were injected into rats in differ ent conditions, and their pineal melatonin contents were measured by radioi mmunoassay. Experiment 1: Blocking the alpha(2)-adrenoceptors and possible non-adrenergic binding sites with atipamezole did not counteract the light- induced suppression of nocturnal melatonin. These receptors are, thus, not essential for the suppression of melatonin by light. Experiment 2: Blocking the alpha(2)-adrenoceptors with atipamezole or yohimbine did not sensitize the pineal melatonin synthesis to daytime darkness in the light/dark-entra ined rats. The binding sites are not involved in keeping the daytime melato nin levels low, even in darkness. Experiment 3: The rats were sensitized to daytime darkness by keeping them for seven days in constant Light. The dar k-elicited melatonin rise was suppressed by a lower dose of medetomidine th an the normal nocturnal rise in light/dark-entrained rats, while atipamezol e had no effect. The results showed that alpha(2)-adrenoceptor insufficiency is not involved in the constant light-induced pineal supersensitivity. In summary, the exp eriments indicated that the physiological regulation of melatonin synthesis by ambient lighting in rats does not depend on alpha(2)-adrenergic mechani sms. (C) 1999 IBRO. Published by Elsevier Science Ltd.