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Titolo:
Differential responsivity of the hypothalamic-pituitary-adrenal axis to glucocorticoid negative-feedback and corticotropin releasing hormone in rats undergoing morphine withdrawal: Possible mechanisms involved in facilitatedand attenuated stress responses
Autore:
Houshyar, H; Galigniana, MD; Pratt, WB; Woods, JH;
Indirizzi:
Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 t Pharmacol, Ann Arbor, MI 48109 USA Univ Michigan, Dept Psychol, Ann Arbor, MI USA Univ Michigan Ann Arbor MIUSA Michigan, Dept Psychol, Ann Arbor, MI USA
Titolo Testata:
JOURNAL OF NEUROENDOCRINOLOGY
fascicolo: 10, volume: 13, anno: 2001,
pagine: 875 - 886
SICI:
0953-8194(200110)13:10<875:DROTHA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA LEVELS; PARAVENTRICULAR NUCLEUS; ACTH-SECRETION; DEXAMETHASONE SUPPRESSION; CORTICOSTERONE RECEPTORS; ADRENOCORTICAL ACTIVITY; NORADRENERGIC ACTIVITY; ANTERIOR-PITUITARY; RESTRAINT STRESS; DRUG-DEPENDENCE;
Keywords:
restraint stress; morphine; dexamethasone; CRH; glucocorticoid receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Houshyar, H Univ Calif San Francisco, Dept Physiol, 513 Parnassus Ave,RoomHSW 750, San Francisco, CA 94143 USA Univ Calif San Francisco 513 Parnassus Ave,Room HSW 750 San Francisco CA USA 94143
Citazione:
H. Houshyar et al., "Differential responsivity of the hypothalamic-pituitary-adrenal axis to glucocorticoid negative-feedback and corticotropin releasing hormone in rats undergoing morphine withdrawal: Possible mechanisms involved in facilitatedand attenuated stress responses", J NEUROENDO, 13(10), 2001, pp. 875-886

Abstract

Chronic morphine treatment produces profound and long-lasting changes in the pituitary-adrenal responses to stressful stimuli. The purpose of the present study was to explore the mechanisms involved in these altered stress responses. Chronic morphine administration increased basal plasma concentrations of corticosterone and adrenocorticotropic hormone (ACTH), which peakedat 36 h after the final morphine injection and returned to normal levels within 84-h. Whole brain glucocorticoid receptor protein expression was reduced (approximately 70%) in morphine-treated rats 4-h after the final morphine injection and these levels recovered within 16-h. Twelve hours followingmorphine withdrawal, rats displayed normal ACTH, but potentiated and prolonged corticosterone responses to restraint stress. Both the ACTH and corticosterone responses to restraint in acutely withdrawn rats were insensitive to dexamethasone. Furthermore, acutely withdrawn rats displayed reduced ACTH but prolonged corticosterone responses to peripheral corticotropin-releasing hormone (CRH) administration. These findings suggest that the normal ACTH and enhanced corticosterone responses to stress in acutely withdrawn rats involved decreased sensitivity of negative-feedback systems to glucocorticoids, reduced pituitary responsivity to CRH, and enhanced sensitivity of the adrenals to ACTH. Eight days following morphine withdrawal, rats displayed dramatically reduced ACTH, but normal corticosterone responses to restraint stress. These rats displayed enhanced sensitivity to dexamethasone and normal pituitary-adrenal responses to CRH. These data suggest that the reduced ACTH responses to stress in 8-day withdrawal rats involved increased sensitivity of negative-feedback systems to glucocorticoids as well as reduced CRH and/or AVP function in response to stress. Taken together, the results of this study illustrate some of the mechanisms mediating altered stress responsivity in rats that have received chronic morphine treatment.

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Documento generato il 22/01/20 alle ore 18:46:29