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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Desensitization of pigment granule aggregation in Xenopus leavis melanophores: melatonin degradation rather than receptor down-regulation is responsible.

Xenopus laevis melanophores express a high density (B(max) 1224 fmol/mg protein) of high-affinity (K(d) 37 pm) cell membrane melatonin receptors. Treatment of melanophores with melatonin resulted in a loss of membrane melatonin receptors reaching a maximum (approximately 60%) by 6 h. In addition to receptor loss, a decline in the potency of melatonin to produce pigment aggregation was observed on prolonged treatment. However, the loss of potency (3.8-fold in 24 h and 162-fold in 96 h) was much slower than loss of receptors, and was completely prevented by inclusion of eserine (100 microm), an inhibitor of melatonin deacetylation in the culture medium. Incubation of melanophores with [(3)H]-melatonin showed that eserine prevented metabolism of melatonin to 5-methoxytryptamine. These results indicate that although receptor density does decline on prolonged treatment, this is not responsible for the diminishing melatonin potency, which is entirely due to degradation of melatonin by deacetylation and subsequent deamination in melanophores.[1]


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