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

• Published in: Biology of reproduction Vol. 71; no. 3; pp. 813 - 819
• Main Authors: Van Vugt, Harmke H, Swarts, Hans J. M, Van de Heijning, Bert J. M, Van der Beek, Eline M
• Format: Journal Article
• Language: English
• Published: 01.09.2004
• Subjects: Contents; gonadotropin-releasing hormone; growth hormone; hypothalamus; luteinizing hormone; ovulatory cycle
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod.104.028936

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.