Author:
Balík A,Jindřichová M,Bhattacharyya S,Zemková H
Abstract
Two forms of gonadotropin-releasing hormone (GnRH), GnRH-I
and GnRH-II, are commonly present in mammals. The main
hormone controlling reproduction is GnRH-I acting through its
receptor (GnRHR-I), whereas the function of GnRH-II is
unknown. In primates, it has been suggested that GnRH-II is a
specific agonist for the structurally distinct GnRHR-II. Here we
compared effects of GnRH-I and GnRH-II on intracellular calcium
and gonadotropin hormone release in neonatal rat gonadotrophs
in vitro and the dependence of agonist actions on cyclic
nucleotide levels. Both agonists elevated intracellular calcium and
stimulated gonadotropin secretion in a concentration-dependent
manner, with comparable peak amplitudes, but GnRH-I was
three times more potent than GnRH-II. Antide, a specific GnRHRI antagonist, completely blocked the action of both agonists on
gonadotropin release. Inhibition of adenylyl cyclase activity by
melatonin and MDL significantly attenuated GnRH-I- and GnRHII-induced calcium signaling and gonadotropin release, whereas
inhibition of soluble guanylyl cyclase activity was ineffective.
GnRH-II also generated calcium oscillations in a fraction of
gonadotrophs not expressing melatonin receptors. These results
indicate that GnRH-I and GnRH-II act on the same GnRHR to
stimulate gonadotropin release through intracellular calcium and
cyclic nucleotide signaling, and that GnRH-II is less potent
agonist for this receptor in neonatal rat gonadotrophs.
Publisher
Institute of Physiology of the Czech Academy of Sciences
Subject
General Medicine,Physiology
Cited by
3 articles.
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