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- W2040835804 abstract "This study was carried out to clarify the role of α2-adrenoceptors in the regulation of pineal melatonin synthesis. Medetomidine, a selective α2-adrenoceptor agonist, was previously found to be a potent suppressor of nocturnal melatonin levels in rats. Medetomidine and α2-adrenoceptor antagonists atipamezole and yohimbine were injected into rats in different conditions, and their pineal melatonin contents were measured by radioimmunoassay. Experiment 1: Blocking the α2-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 α2-adrenoceptors with atipamezole or yohimbine did not sensitize the pineal melatonin synthesis to daytime darkness in the light/dark-entrained rats. The binding sites are not involved in keeping the daytime melatonin levels low, even in darkness. Experiment 3: The rats were sensitized to daytime darkness by keeping them for seven days in constant light. The dark-elicited melatonin rise was suppressed by a lower dose of medetomidine than the normal nocturnal rise in light/dark-entrained rats, while atipamezole had no effect. The results showed that α2-adrenoceptor insufficiency is not involved in the constant light-induced pineal supersensitivity. In summary, the experiments indicated that the physiological regulation of melatonin synthesis by ambient lighting in rats does not depend on α2-adrenergic mechanisms." @default.
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- W2040835804 date "1999-06-01" @default.
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- W2040835804 title "Evidence against alpha2-adrenoceptor involvement in the regulation of rat melatonin synthesis by ambient lighting" @default.
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- W2040835804 doi "https://doi.org/10.1016/s0306-4522(99)00057-3" @default.
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