Submitted January 20, 2004
Returned for revision February 11, 2004
Accepted March 18, 2004
Neuroendocrinology
Evidences for Different Gonadotropin-Releasing Hormone
Response Sites in Rat Ovarian and Pituitary Cells
Lucas A. Mongiat ,
Victoria A. Lux-Lantos ,
and
Carlos Libertun *
* To whom correspondence should be addressed. E-mail: libertun{at}dna.uba.ar.
Abstract
The participation of type I GnRH receptor on GnRH-II-induced gonadotropin secretion in rat pituitary cells was investigated. Furthermore, we extended the study of GnRH-II action to ovarian cells. GnRH-II was able to mobilize IP3 and to induce LH and FSH release in a dose-dependent manner in pituitary cells and in a GnRH-I-like manner. The GnRH analog 135-18 (agonist for type II GnRH receptor and antagonist for type I GnRH receptor) was unable to elicit any cellular response tested in these pituitary cells. GnRH-II responses were blocked by the type I GnRHR antagonists Cetrorelix or 135-18, suggesting that these effects were mediated by the type I GnRH receptor. In contrast to pituitary cells, GnRH-I but not GnRH-II, elicited an IP3 response in superovulated ovarian cells; 135-18 had no effect either. However GnRH-II as well as GnRH-I presented anti-proliferative effects on these cells. Surprisingly, 135-18 had stronger anti-proliferative effects than either GnRH peptide. The 135-18 analog, but not GnRH-I or GnRH-II, increased progesterone secretion in superovulated ovarian cells. These results strongly suggest that GnRH-II is able to stimulate rat pituitary cells through the type I GnRH receptor with no evidence of type II GnRH receptor presence. On the other hand, our results indicate that there is a putative GnRH receptor in superovulated ovarian cells with different response characteristics than the GnRH receptor in the pituitary.
Key words:
Neuroendocrinology •
Ovary •
Pituitary •
Gonadotropin-releasing hormone •
Gonadotropin-releasing hormone receptor
