HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 71/3/813    most recent biolreprod.104.028936v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Van Vugt, H. H. Articles by Van der Beek, E. M. Search for Related Content PubMed PubMed Citation Articles by Van Vugt, H. H. Articles by Van der Beek, E. M. Agricola Articles by Van Vugt, H. H. Articles by Van der Beek, E. M.

Centrally Applied Somatostatin Inhibits the Estrogen-Induced Luteinizing Hormone Surge via Hypothalamic Gonadotropin-Releasing Hormone Cell Activation in Female Rats¹

Human and Animal Physiology Group,³ Animal Sciences Group, Wageningen University, 6709 PJ, Wageningen, The Netherlands Numico Research,⁴ Department of Biomedical Research, 6700 CA, Wageningen, The Netherlands

Overexpression of growth hormone (GH) as well as GH-deficiency dramatically impairs reproductive function. Decreased reproductive function as a result of altered GH release is, at least partially, due to changes at the hypothalamic-pituitary level. We hypothesize that hypothalamic somatostatin (SOM), the inhibiting factor of GH release from the pituitary, may play a central role in the "crosstalk" between the somatotropic and gonadotropic axes. In the present study we investigated the possible effects of a centrally applied SOM analog on the LH surge and the concurrent activation of hypothalamic GnRH neurons in female rats. To this end, female rats were treated with estradiol 2 wk after ovariectomy and were given a single central injection with either the SOM analog, octreotide, or saline just prior to surge onset, after which hourly blood samples were taken to measure LH. Two weeks later, the experimental setup was randomly repeated to collect brains during the anticipated ascending phase of the LH surge. Vibratome sections were subsequently double-stained for GnRH and cFos peptide. Following octreotide treatment, LH surges were significantly attenuated compared to those in saline-treated control females. Also, octreotide treatment significantly decreased the activation of hypothalamic GnRH neurons. These results clearly demonstrate that SOM is able to inhibit LH release, at least in part by decreasing the activation of GnRH neurons. Based on these results, we hypothesize that hypothalamic SOM may be critically involved in the physiological regulation of the proestrus LH surge.

¹ This work was supported by the Wageningen Institute of Animal Sciences, Graduate School of Wageningen University.

² Correspondence: Harmke H. Van Vugt, Human and Animal Physiology Group, Animal Sciences Group, Wageningen University, Haarweg 10, 6709 PJ Wageningen, The Netherlands. FAX: 31 317 484077; harmke.vanvugt{at}wur.nl

This article has been cited by other articles:

				J. Robinson Prenatal programming of the female reproductive neuroendocrine system by androgens. Reproduction, October 1, 2006; 132(4): 539 - 547. [Abstract] [Full Text] [PDF]