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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 facilitated and attenuated stress responses.
J Neuroendocrinol 2001; 13(10):875-86JN

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 peaked at 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 following morphine 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 Both the ACTH and corticosterone responses to restraint in acutely withdrawn rats were insensitive to dexamethasone. Furthermore, acutely withdrawn rats displayed reduced ACTH but prolonged corticosterone responses to peripheral corticotropin releasing hormone (CRH) administration. These findings suggest that the normal ACTH and enhanced corticosterone responses to stress in acutely withdrawn rats involved decreased sensitivity of negative-feedback systems to glucocorticoids, reduced pituitary responsivity to CRH, and enhanced sensitivity of the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.

Authors+Show Affiliations

Department of Pharmacology, University of Michigan, Ann Arbor, MI, USA. hani@itsa.ucsf.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11679056

Citation

Houshyar, H, 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 Facilitated and Attenuated Stress Responses." Journal of Neuroendocrinology, vol. 13, no. 10, 2001, pp. 875-86.
Houshyar H, Galigniana MD, Pratt WB, 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 facilitated and attenuated stress responses. J Neuroendocrinol. 2001;13(10):875-86.
Houshyar, H., Galigniana, M. D., Pratt, W. B., & Woods, J. H. (2001). 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 facilitated and attenuated stress responses. Journal of Neuroendocrinology, 13(10), pp. 875-86.
Houshyar H, 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 Facilitated and Attenuated Stress Responses. J Neuroendocrinol. 2001;13(10):875-86. PubMed PMID: 11679056.
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TY - JOUR T1 - 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 facilitated and attenuated stress responses. AU - Houshyar,H, AU - Galigniana,M D, AU - Pratt,W B, AU - Woods,J H, PY - 2001/10/27/pubmed PY - 2002/1/5/medline PY - 2001/10/27/entrez SP - 875 EP - 86 JF - Journal of neuroendocrinology JO - J. Neuroendocrinol. VL - 13 IS - 10 N2 - 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 peaked at 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 following morphine 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. SN - 0953-8194 UR - https://www.unboundmedicine.com/medline/citation/11679056/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_facilitated_and_attenuated_stress_responses_ L2 - https://doi.org/10.1046/j.1365-2826.2001.00714.x DB - PRIME DP - Unbound Medicine ER -