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Provedor de dados:  Inra
País:  France
Título:  Endotoxin inhibits the surge secretion of gonadotropin-releasing hormone via a prostaglandin-independent pathway
Autores:  Breen, K.M.
Billings, H. J.
Debus, N.
Karsch, F. J.
Data:  2004
Ano:  2004
Palavras-chave:  ENDOTOXINE
HORMONE GONADOTROPE
GONADOTROPINE
PROSTAGLANDINE
SECRETION DE LH
PULSE DE GNRH
CYCLE OVARIEN
HYPOTHALAMUS ENDOTOXIN
HORMONE
GONADOTROPIN
GNRH
LH
Resumo:  Immune/inflammatory challenges, such as bacterial endotoxin, disrupt gonadotropin secretion and ovarian cyclicity. We previously determined that endotoxin can block the estradiol-induced LH surge in the ewe. Here, we investigated mechanisms underlying this suppression. First, we tested the hypothesis that endotoxin blocks the estradiol-induced LH surge centrally, by preventing the GnRH surge. Artificial follicular phases were created in ovariectomized ewes, and either endotoxin or vehicle was administered together with a surge-inducing estradiol stimulus. In each ewe in which endotoxin blocked the LH surge, the GnRH surge was also blocked. Given this evidence that endotoxin blocks the estradiol-induced LH surge at the hypothalamic level, we began to assess underlying central mechanisms. Specifically, in view of the prior demonstration that prostaglandins mediate endotoxin-induced suppression of pulsatile GnRH secretion in ewes, we tested the hypothesis that prostaglandins also mediate endotoxin-induced blockade of the surge. The prostaglandin synthesis inhibitor flurbiprofen was delivered together with endotoxin and the estradiol stimulus. Although flurbiprofen abolished endotoxin-induced fever, which is a centrally generated, prostaglandin-mediated response, it failed to reverse blockade of the LH surge. Collectively, these results indicate endotoxin blocks the LH surge centrally, suppressing GnRH secretion via a mechanism not requiring prostaglandins. This contrasts with the suppressive effect of endotoxin on GnRH pulses, which requires prostaglandins as intermediates.
Tipo:  Journal Article
Idioma:  Inglês
Identificador:  http://www.prodinra.inra.fr/prodinra/pinra/doc.xsp?id=PROD2007a6a7a3a2&uri=/notices/prodinra1/2008/09/
Fonte:  Endocrinology. 2004, 145 (1) : 221-227
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