Evidence for different gonadotropin-releasing hormone response sites in rat ovarian and pituitary cells

The participation of type I GnRH receptor (GnRH-R) on GnRH-II-induced gonadotropin secretion in rat pituitary cells was investigated. Furthermore, we extended the study of GnRH-II action to ovarian cells. The GnRH-II was able to mobilize inositol triphosphate (IP3) and to induce LH and FSH release i...

Descripción completa

Guardado en:
Detalles Bibliográficos
Publicado: 2004
Materias:
Gonadotropin-releasing hormone
Gonadotropin-releasing hormone receptor
Neuroendocrinology
Ovary
Pituitary
gonadorelin
gonadorelin derivative
gonadorelin receptor
inositol trisphosphate
animal cell
article
cell proliferation
concentration response
controlled study
female
follitropin release
gonadotropin release
hormonal regulation
hormone action
hypophysis cell
luteinizing hormone release
neuroendocrinology
nonhuman
ovary cell
priority journal
progesterone release
rat
superovulation
Animals
Cells, Cultured
Female
Follicle Stimulating Hormone
Gonadotropin-Releasing Hormone
Hormone Antagonists
Luteinizing Hormone
Pituitary Gland, Anterior
Rats
Rats, Sprague-Dawley
Receptors, LHRH
Superovulation
Animalia
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00063363_v71_n2_p464_Mongiat
http://hdl.handle.net/20.500.12110/paper_00063363_v71_n2_p464_Mongiat
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:The participation of type I GnRH receptor (GnRH-R) on GnRH-II-induced gonadotropin secretion in rat pituitary cells was investigated. Furthermore, we extended the study of GnRH-II action to ovarian cells. The GnRH-II was able to mobilize inositol triphosphate (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-R and antagonist for type I GnRH-R) was unable to elicit any cellular response tested in these pituitary cells. The GnRH-II responses were blocked by the type I GnRH-R-antagonists CRX or 135-18, suggesting that these effects were mediated by the type I GnRH-R. In contrast to pituitary cells, GnRH-I, but not GnRH-II, elicited an IP3 response in superovulated ovarian cells; 135-18 also had no effect. However, GnRH-II as well as GnRH-I presented antiproliferative effects on these cells. Surprisingly, 135-18 had stronger antiproliferative 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-R, with no evidence for the presence of type II GnRH-R. On the other hand, our results indicate a putative GnRH-R in superovulated ovarian cells with response characteristics that differ from those of the GnRH-R in the pituitary.

Ejemplares similares