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Titolo:
TESTOSTERONE ACTS DIRECTLY AT THE PITUITARY TO REGULATE GONADOTROPIN-RELEASING HORMONE-INDUCED CALCIUM SIGNALS IN MALE-RAT GONADOTROPES
Autore:
TOBIN VA; MILLAR RP; CANNY BJ;
Indirizzi:
MONASH UNIV,DEPT PHYSIOL CLAYTON VIC 3168 AUSTRALIA MONASH UNIV,DEPT PHYSIOL CLAYTON VIC 3168 AUSTRALIA UNIV CAPE TOWN,DEPT CHEM PATHOL,RES UNIT MOL REPROD ENDOCRINOL ZA-7700 RONDEBOSCH SOUTH AFRICA
Titolo Testata:
Endocrinology
fascicolo: 8, volume: 138, anno: 1997,
pagine: 3314 - 3319
SICI:
0013-7227(1997)138:8<3314:TADATP>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOLLICLE-STIMULATING-HORMONE; SUBUNIT GENE-EXPRESSION; LUTEINIZING-HORMONE; SECRETION; CELLS; RESPONSES; MOBILIZATION; PROGESTERONE; OSCILLATIONS; MODULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
V.A. Tobin et al., "TESTOSTERONE ACTS DIRECTLY AT THE PITUITARY TO REGULATE GONADOTROPIN-RELEASING HORMONE-INDUCED CALCIUM SIGNALS IN MALE-RAT GONADOTROPES", Endocrinology, 138(8), 1997, pp. 3314-3319

Abstract

We have recently shown that castration alters GnRH-induced calcium (Ca2+) signaling in the gonadotropes of male rats. Instead of generatingspike-plateau Ca2+ responses to high concentrations of GnRH (100 nM),the majority of gonadotropes from castrated rats have oscillatory Ca2 responses, which are generally only seen with low concentrations of GnRH in the gonadotropes of intact rats. This change in the nature of GnRH-induced Ca2+ responses is prevented by in vivo testosterone treatment. The aims of the present study were, therefore, to determine if testosterone acts directly at the pituitary or via the regulation of hypothalamic GnRH secretion. Accordingly, castrated male rats were treated with a GnRH antagonist to ablate the effects of increased GnRH secretion at the pituitary gland. GnRH antagonist treatment (10 mu g/100 gBW, twice daily for 7 days from the time of castration) decreased theconcentration of LH in the serum of castrated rats (0.4 +/- 0.1 ng/mlcs. 11.2 +/- 0.4 ng/ml in untreated castrated rats, mean +/- SEM) buthad no effect on the proportion of gonadotropes having oscillatory Ca2+ responses to 100 nM GnRH when compared with untreated castrated rats (63% in antagonist-treated castrated rats vs. 70% in untreated castrated rats). The GnRH antagonist treatment did not, however, interfere with the ability of in vivo testosterone treatment (100 mu g/100 g body weight/day) to decrease the proportion of gonadotropes having oscillatory Ca2+ responses to 100 nM GnRH (26% in testosterone-treated rats vs. 25% in testosterone and antagonist-treated rats). These findings indicate that testosterone acts directly at the pituitary, and not by altered GnRH secretion, to modulate GnRH-induced Ca2+ signals. To confirm this suggestion, cultured gonadotropes of castrated male rats were treated in vitro with 10 nM testosterone. Testosterone treatment for twelve, but not 4 h, restored the proportion of gonadotropes having oscillatory Ca2+ responses to that seen in gonadotropes from intact rats. The in vitro affects of testosterone over 12 h were prevented by concomitant treatment with the protein synthesis inhibitor cycloheximide (10 mu M), which, when given alone, had no effect on GnRH-induced Ca2+ signals in cells from castrate male rats. Taken together, these findings suggest that testosterone has a direct genomic action at the pituitary to regulate GnRH-induced Ca2+ signals, via a process that involvesnew protein synthesis.

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Documento generato il 28/09/20 alle ore 15:43:24