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• W2043874391 startingPage "99" @default.
• W2043874391 abstract "The hormone melatonin is an output signal of an endogenous circadian clock in retinal photoreceptors. Melatonin may act as a paracrine and/or intracrine neurohormone by binding to specific receptors in the eye. The distribution of Mel1a and Mel1c melatonin receptors in the Xenopus laevis retina was examined by immunocytochemistry, using antibodies prepared against specific sequences of the Xenopus receptor proteins. Antibodies that label dopaminergic and GABA-ergic amacrine cells were used in double-label experiments with the melatonin receptor antibodies. The distribution of Mel1a and Mel1c receptor immunoreactivity was similar insofar as the two receptors were localized in the inner plexiform layer. However, the Mel1c receptor displayed some immunoreactivity in the photoreceptor cells, whereas the Mel1a receptor displayed little if any photoreceptor labelling. The Mel1c antibody, but not the Mel1a, labelled a population of ganglion cells. While both receptors were localized to the outer plexiform layer, they did not appear to localize to the identical cell types. These results demonstrate that the Mel1a and Mel1c receptor proteins are present in cells of the X. laevis retina, and their distribution in the photoreceptors and inner retina is very similar to that reported in the human retina. The differential pattern of expression of the melatonin receptors suggests that melatonin may convey differential effects on various target cells in the retina." @default.
• W2043874391 created "2016-06-24" @default.
• W2043874391 creator A5061151961 @default.
• W2043874391 date "2003-01-01" @default.
• W2043874391 modified "2023-09-27" @default.
• W2043874391 title "Differential distribution of Mel1a and Mel1c melatonin receptors in Xenopus laevis retina" @default.
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• W2043874391 doi "https://doi.org/10.1016/s0014-4835(02)00230-0" @default.
• W2043874391 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12589779" @default.
• W2043874391 hasPublicationYear "2003" @default.
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