Abstract
Dopamine significantly decreased melatonin levels in Golden hamster retinas excised at noon and incubated under light. The effect of dopamine was reversed by spiperone and clozapine (selective antagonists for D2 and for D4/D2dopaminergic receptors, respectively) but not by SCH 23390 (a selective D1 dopamine receptor antagonist). Both clozapine and spiperone per se significantly increased melatonin levels, whereas SCH 23390 was ineffective. Quinpirole (an agonist for D2-subfamily dopaminergic receptor) decreased melatonin content in retinas excised at midday. Dopamine increased, whereas quinpirole decreased, cAMP accumulation in retinas excised at noon. Retinal dopaminergic turnover rate (assessed as the ratio of 3,4-dihydroxyphenylacetic acid to dopamine) was significantly higher at midday than at midnight. In retinas excised at midnight, melatonin content in vitro was unaffected by dopamine or quinpirole. At midnight, dopamine increased cAMP accumulation, whereas quinpirole was ineffective. When hamsters were kept under constant darkness for 48 h and sacrificed at subjective midday or midnight, dopamine increased cAMP accumulation at both times, whereas quinpirole decreased this parameter only at subjective midday. Dopaminergic turnover rate was significantly higher at subjective midday than at subjective midnight. These results show that dopamine regulates melatonin biosynthesis in the Golden hamster retina.
Footnotes
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Send reprint requests to: Dr. Ruth E. Rosenstein, Departamento de Bioquı́mica Humana, Facultad de Medicina, UBA, Paraguay 2155, 5°P (1121), Buenos Aires, Argentina. E-mail:ruthr{at}fmed.uba.ar
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↵1 This research was supported by grants from Fundación Antorchas, Consejo Nacional de Investigaciones Cientı́ficas y Técnicas (CONICET), and Universidad de Buenos Aires, Argentina.
- Abbreviations:
- NAT
- N-acetyltransferase, IBMX, 3-isobutyl-1-methylxanthine
- DOPAC
- 3,4-dihydroxyphenylacetic acid
- DHBA
- 3,4-dihydroxybenzylamine
- RIA
- radioimmunoassay
- Received July 1, 1999.
- Accepted December 27, 1999.
- The American Society for Pharmacology and Experimental Therapeutics
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