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J. Biol. Chem., Vol. 277, Issue 1, 251-258, January 4, 2002
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From the Melatonin plays a significant role in the control
of the hypothalamic-pituitary-gonadal axis. Using the GT1-7 cell line,
an in vitro model of GnRH-secreting neurons of the
hypothalamus, we examined the potential signal transduction pathways
activated by melatonin directly at the level of the GT1-7 neuron. We
found that melatonin inhibits forskolin-stimulated adenosine 3'-,
5'-cyclic monophosphate accumulation in GT1-7 cells through an
inhibitory G protein. Melatonin induced protein kinase C activity by
1.65-fold over basal levels, increased the phosphorylation of
extracellular signal-regulated kinase 1 and 2 proteins, and activated
c-fos and junB mRNA expression in GT1-7
cells. Using the protein kinase A inhibitor H-89, the protein kinase C
inhibitor bisindolylmaleimide, and the mitogen-activated protein kinase
kinase inhibitor PD98059, we found that the melatonin-mediated cyclical
regulation of GnRH mRNA expression may involve the protein kinase C
and the extracellular signal-regulated kinase 1 and 2 pathways, but not
the protein kinase A pathway. We found that melatonin suppresses GnRH
secretion by ~45% in the GT1-7 neurons. However, in the presence of
the inhibitors H-89, bisindolylmaleimide, and PD98059 melatonin was unable to suppress GnRH secretion. These results provide insights into
the potential signal transduction mechanisms involved in the control of
GnRH gene expression and secretion by melatonin.
Melatonin Receptor Activation Regulates GnRH Gene Expression and
Secretion in GT1-7 GnRH Neurons
SIGNAL TRANSDUCTION MECHANISMS*
and§¶
Institute for Medical Sciences and the
§ Department of Physiology, University of Toronto, and the
¶ Division of Cellular and Molecular Biology, University Health
Network, Toronto, Ontario M5S 1A8, Canada
*
This work was supported by a Natural Science and Engineering
Research Council Operating Grant (to D. D. B.) and an Ontario Graduate Scholarship in Science and Technology (to D. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Canadian Institutes of Health Research Scholar and
a Canada Foundation for Innovation Researcher. To whom correspondence
should be addressed: Dept. of Physiology, Univ. of Toronto, Medical
Sciences Bldg., Rm. 3247A, 1 King's College Circle, Toronto, Ontario
M5S 1A8, Canada. Tel.: 416-946-7646; Fax: 416-978-4940; E-mail:
d.belsham@utoronto.ca.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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