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Titolo:
Hypocretin/orexin suppresses corticotroph responsiveness in vitro
Autore:
Samson, WK; Taylor, MM;
Indirizzi:
St Louis Univ, Sch Med, St Louis, MO 63104 USA St Louis Univ St Louis MO USA 63104 Univ, Sch Med, St Louis, MO 63104 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
fascicolo: 4, volume: 281, anno: 2001,
pagine: R1140 - R1145
SICI:
0363-6119(200110)281:4<R1140:HSCRIV>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; RECEPTOR MESSENGER-RNA; HYPOTHALAMIC NEUROPEPTIDES; OREXIN-A; LUTEINIZING-HORMONE; ANTERIOR-PITUITARY; RAT-BRAIN; SECRETION; ADRENOCORTICOTROPIN; OREXIN/HYPOCRETIN;
Keywords:
adrenocorticotropin; pituitary; hypothalamus; hypocretin; orexin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Samson, WK 1402 S Grand Blvd, St Louis, MO 63104 USA 1402 S Grand Blvd StLouis MO USA 63104 St Louis, MO 63104 USA
Citazione:
W.K. Samson e M.M. Taylor, "Hypocretin/orexin suppresses corticotroph responsiveness in vitro", AM J P-REG, 281(4), 2001, pp. R1140-R1145

Abstract

The hypocretin/orexins (Hcrts/ORXs) are peptides produced in neurons in the lateral hypothalamic area that project to neuroendocrine centers in the hypothalamus. Hcrt/ORX receptors are present in the hypothalamus and anterior pituitary gland. We examined the possibility that the Hcrts/ORXs, which we have demonstrated previously to act in the brain to stimulate sympatheticfunction, could alter stress hormone secretion by a direct pituitary action. In vitro studies revealed a dose-related inhibitory effect of the Hcrts/ORXs on corticotropin-releasing hormone-stimulated ACTH secretion that appeared to be mediated via the orexin-1 receptor and to be expressed at doses (threshold dose 1 nM orexin A) similar to the affinity constant for the receptor. The effect was not due to abrogation of the cAMP response of the corticotroph to corticotropin-releasing hormone and was not pertussis toxin sensitive, suggesting a non-G(i)-mediated mechanism. Instead, a G(q)-mediatedsignaling mechanism was indicated by the ability of protein kinase C blockade with calphostin C to reverse the inhibitory action of orexin A. Orexin A and orexin B did not significantly alter basal ACTH secretion in vitro and did not alter basal or releasing factor-stimulated secretion of luteinizing hormone, prolactin, thyroid-stimulating hormone or growth hormone from cells harvested from male or random-cycle female donors. Our data suggest a direct, pituitary action of the Hcrts/ ORXs to modulate the endocrine response to stress and identify the potential cellular mechanism of a unique biological action of the peptides in the anterior pituitary gland.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/01/20 alle ore 12:19:02