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Titolo:
Regulation of the hypothalamic-pituitary-adrenocortical system in mice deficient for CRH receptors 1 and 2
Autore:
Preil, J; Muller, MB; Gesing, A; Reul, JMHM; Sillaber, I; van Gaalen, MM; Landgrebe, J; Holsboer, F; Stenzel-Poore, M; Wurst, W;
Indirizzi:
Max Planck Inst Psychiat, D-80804 Munich, Germany Max Planck Inst Psychiat Munich Germany D-80804 D-80804 Munich, Germany Inst Mammalian Genet, GSF Res Ctr, D-85764 Munich, Germany Inst Mammalian Genet Munich Germany D-85764 Ctr, D-85764 Munich, Germany Oregon Hlth Sci Univ, Dept Mol Microbiol & Immunol, Portland, OR 97201 USAOregon Hlth Sci Univ Portland OR USA 97201 mmunol, Portland, OR 97201 USA
Titolo Testata:
ENDOCRINOLOGY
fascicolo: 11, volume: 142, anno: 2001,
pagine: 4946 - 4955
SICI:
0013-7227(200111)142:11<4946:ROTHSI>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORTICOTROPIN-RELEASING-HORMONE; IMPAIRED STRESS-RESPONSE; ANTISENSE OLIGODEOXYNUCLEOTIDE; CHRONIC INFUSION; ADRENAL-MEDULLA; REDUCED ANXIETY; UROCORTIN; BEHAVIOR; HORMONE-RECEPTOR-1; GLUCOCORTICOIDS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Wurst, W Max Planck Inst Psychiat, Mol Neurogenet Karepelinstr 2-10, D-80804 Munich, Germany Max Planck Inst Psychiat Mol Neurogenet Karepelinstr 2-10 Munich Germany D-80804
Citazione:
J. Preil et al., "Regulation of the hypothalamic-pituitary-adrenocortical system in mice deficient for CRH receptors 1 and 2", ENDOCRINOL, 142(11), 2001, pp. 4946-4955

Abstract

Recent investigations in mouse lines either deficient for the CRH receptor1 (CRHR1) or 2 (CRHR2) suggest that the CRH neuronal system may comprise two separate pathways that can be coordinately and inversely activated in stress-induced hypothalamic-pituitary-adrenal (EPA) response and anxiety-likebehavior. We generated mice deficient for both CRHR1 (Crhr1(-/-)) and CRHR2 (Crhr2(-/-)) to investigate the HPA system regulation in the absence of known functionally active CRH receptors under basal conditions and in response to different ethologically relevant stressors. To elucidate possible gene dose effects on the action of both CRH receptors, our analysis included heterozygous and homozygous CRHR1- or CRHR2-deficient mice, mutants lacking both CRH receptors, compound mutants with homozygous and heterozygous deficiency for either of the receptors, and their wild-type littermates. Both male and female Crhr1(-/-)Crhr2(-/-) mutants were viable, fertile, and indistinguishable in size from wild-type littermates. We show that the endocrine phenotype of mice lacking both CRHRs is dominated by the functional loss ofCRHR1. CRHR2 does not compensate for CRHR1 deficiency, nor does the lack of CRHR2 exacerbate the CRHR1-dependent impairment of the HPA system function. Within the intraadrenal CRH/ACTH system, our data suggest different roles for CRHR1 and CRHR2 in fine-tuning of adrenocortical corticosterone release.

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Documento generato il 07/07/20 alle ore 19:07:30