Endocrinology, Vol 121, 190-199, Copyright © 1987 by Endocrine Society

ARTICLES

Steroid effects on the secretory modalities of gonadotropin-releasing hormone release

P Melrose and L Gross

GnRH neurons isolated immunochemically from the brain of adult male rats were used to determine whether testosterone (T), dihydrotestosterone (DHT), estradiol-17 beta (E(2)17 beta), 20H-estrone (OHE1), or progesterone (P4) have a direct effect on the spontaneous neurosecretion and/or cellular content of GnRH. Neurons harvested from individual rats were treated with a single steroid pulse; samples were collected before treatment, during the steroid pulse, and at 24 h post treatment. Androgen treatments of 100 pg/ml or 1 ng/ml media elicited an increase in GnRH pulse frequency 1-6 min after steroid exposure without affecting the amplitude of release; these modalities persisted at 2 h. The frequency of GnRH pulses was increased 24 h after the neurons received the brief 100 pg/ml or 1 ng/ml T or 1 ng/ml DHT treatments. Neurons exposed to androgen treatments also appeared to express large amplitude GnRH pulses infrequently at this time whereas there was no androgen affect on the cellular GnRH concentration. In contrast, E(2)17 beta, OHE1, and P4 treatments had no affect on the mean media GnRH concentration, baseline GnRH concentration, or on the frequency and amplitude of GnRH pulses at any time point. However, the 1 ng/ml P4 and the 1 ng/ml OHE1 treatments both reduced cellular GnRH content at 48 h post treatment. These results suggest that T and DHT may specifically interact with GnRH neurons to elicit immediate and/or long-term changes in the modalities of neuropeptide release and that under physiological conditions GnRH neurons of adult male rats are not directly influenced by E(2)17 beta, the catecholestrogen OHE1, or P4.

This article has been cited by other articles:

				G. Rasier, A.-S. Parent, A. Gerard, M.-C. Lebrethon, and J.-P. Bourguignon Early Maturation of Gonadotropin-Releasing Hormone Secretion and Sexual Precocity after Exposure of Infant Female Rats to Estradiol or Dichlorodiphenyltrichloroethane Biol Reprod, October 1, 2007; 77(4): 734 - 742. [Abstract] [Full Text] [PDF]

				S.K. Blank, C.R. McCartney, and J.C. Marshall The origins and sequelae of abnormal neuroendocrine function in polycystic ovary syndrome Hum. Reprod. Update, July 1, 2006; 12(4): 351 - 361. [Abstract] [Full Text] [PDF]

				T. R. Pak, W. C. J. Chung, J. L. Roberts, and R. J. Handa Ligand-Independent Effects of Estrogen Receptor {beta} on Mouse Gonadotropin-Releasing Hormone Promoter Activity Endocrinology, April 1, 2006; 147(4): 1924 - 1931. [Abstract] [Full Text] [PDF]

				V. MATAGNE, M.-C. LEBRETHON, A. GERARD, and J.-P. BOURGUIGNON In Vitro Paradigms for the Study of GnRH Neuron Function and Estrogen Effects Ann. N.Y. Acad. Sci., December 1, 2003; 1007(1): 129 - 142. [Abstract] [Full Text] [PDF]

				C. L. Pastor, M. L. Griffin-Korf, J. A. Aloi, W. S. Evans, and J. C. Marshall Polycystic Ovary Syndrome: Evidence for Reduced Sensitivity of the Gonadotropin-Releasing Hormone Pulse Generator to Inhibition by Estradiol and Progesterone J. Clin. Endocrinol. Metab., February 1, 1998; 83(2): 582 - 590. [Abstract] [Full Text]