Central melatonin receptors in the rainbow trout: Comparative distribution of ligand binding and gene expression

To better define the role of melatonin in fish, we have compared in detail the distribution of 2‐[125I]iodomelatonin binding sites with gene expression for melatonin receptor subtypes in a widely studied seasonal species, the rainbow trout. Three distinct partial sequences of the melatonin receptor...

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Veröffentlicht in:Journal of comparative neurology (1911) 1999-06, Vol.409 (2), p.313-324
Hauptverfasser: Mazurais, David, Brierley, Ian, Anglade, Isabelle, Drew, Janice, Randall, Clive, Bromage, Niall, Michel, Denis, Kah, Olivier, Williams, Lynda M.
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Sprache:eng
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Zusammenfassung:To better define the role of melatonin in fish, we have compared in detail the distribution of 2‐[125I]iodomelatonin binding sites with gene expression for melatonin receptor subtypes in a widely studied seasonal species, the rainbow trout. Three distinct partial sequences of the melatonin receptor gene were cloned from trout genomic DNA. Two of the sequences corresponded to the Mel1a receptor subtype, and one corresponded to the Mel1b receptor subtype. Analysis of numerous clones failed to find a sequence equivalent to the Mel1c receptor subtype. Comparison of receptor gene expression with 2‐[125I]iodomelatonin binding distribution indicated dendritic transport of the receptor. Melatonin receptors were associated predominantly with visually related areas of the trout brain, such as the thalamic region, the pretectal area, and the optic tectum. The pituitary was devoid of 2‐[125I]iodomelatonin binding, and melatonin receptor gene expression was not detectable. It would appear from the results of the present study that melatonin in this species is involved primarily in the processing of visual signals. How melatonin interacts with circannual rhythms of growth and reproduction is unclear, although a direct interaction between melatonin and the hypothalamopituitary axis is not clearly indicated. J. Comp. Neurol. 409:313–324, 1999. © 1999 Wiley‐Liss, Inc.
ISSN:0021-9967
1096-9861
DOI:10.1002/(SICI)1096-9861(19990628)409:2<313::AID-CNE11>3.0.CO;2-1