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The Human MT 1 Melatonin Receptor Stimulates cAMP Production in the Human Neuroblastoma Cell Line SH‐SY5Y Cells Via a Calcium‐Calmodulin Signal Transduction Pathway
Author(s) -
Schuster C.,
Williams L. M.,
Morris A.,
Morgan P. J.,
Barrett P.
Publication year - 2005
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2005.01288.x
Subject(s) - melatonin , forskolin , melatonin receptor , endocrinology , medicine , signal transduction , biology , sh sy5y , calmodulin , receptor , retinoic acid , cell culture , microbiology and biotechnology , calcium , neuroblastoma , stimulation , genetics
Melatonin regulates circadian and seasonal physiology via melatonin receptors expressed in the brain. However, little is known about the signal transduction mechanisms that mediate the action of melatonin in neuronal cells. To begin to address this issue, we expressed the human MT 1 receptor in the human neuroblastoma SH‐SY5Y cell line. In this cell line, melatonin acutely stimulated cAMP synthesis through a calcium‐calmodulin dependent pathway. This stimulatory effect was independent of an interaction with G i or G s G proteins and dependent upon internal calcium stores. Melatonin also potentiated forskolin‐activated cAMP synthesis. Differentiation of the neuroblastoma cells with retinoic acid to the neuronal phenotype did not alter the ability of melatonin to acutely stimulate cAMP. These data may be relevant to the neuronal action of melatonin and highlight the importance of the cellular context of expression of melatonin and other G protein‐coupled receptors.

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