Involvement of the ganglion cholinergic receptors in gonadotropin-releasing hormone, catecholamines, and progesterone release in the rat ovary
Ganglionic cholinergic stimulation produces changes in ovarian release of progesterone, gonadotropin-releasing hormone, noradrenaline, and adrenaline; the ovarian nerve plexus regulates these mechanisms through the release of different neurotransmitters.
Cristina Daneri, B., Lic., Adriana Vega Orozco, Ph.D., Daniela Bronzi, Claudia Mohn, Ph.D., Ana M. Rastrilla, Ph.D., Zulema Y. Sosa, Ph.D.
Volume 99, Issue 7, Pages 2062-2070, June 2013
To investigate whether cholinergic ganglionic stimulus modifies the release of gonadotropin-releasing hormone (GnRH), catecholamines, and progesterone at the ovarian level.
University animal laboratory.
Six to eight virgin adult Holtzman rats.
Superior mesenteric ganglion–ovarian nerve plexus–ovary system removed and placed in one cuvette with two compartments, with acetylcholine added to the ganglion in the experimental group.
Main Outcome Measure(s):
Measurement of ovarian liquid obtained from catecholamines by high-performance liquid chromatography; measurement of progesterone (P4), GnRH, and luteinizing hormone (LH) by radioimmunoassay; and measurement of gene expression of 3β-hydroxysteroid dehydrogenase (3β-HSD) and 20α-hydroxysteroid dehydrogenase (20α-HSD) by reverse-transcriptase polymerase chain reaction (RT-PCR).
The study focused on the estrus and diestrus II (DII) stages. On the estrus days, the release of GnRH, NA, and 20α-HSD increased, while P4 and 3β-HSD decreased. On the DII days, GnRH, P4, and 3β-HSD increased, while 20α-HSD and NA decreased. The ovarian liquid with GnRH showed biologic activity, namely, an increase in LH release during the DII stage and a decrease during the estrus stage.
Neural stimulus from the superior mesenteric ganglion influences the release of NA, adrenaline, and GnRH. We also have demonstrated that these neurotransmitters participate in the atretogenic processes of the ovary, thus providing evidence of the necessity of the sympathetic neural pathway.
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