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Morphine withdrawal activates hypothalamic-pituitary-adrenal axis and heat shock protein 27 in the left ventricle: the role of extracellular signal-regulated kinase

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dc.contributor.authorHurle, M. A.
dc.contributor.authorAlmela Rojo, Pilar
dc.contributor.authorMartínez Laorden, Elena
dc.contributor.authorMilanés Maquilón, María Victoria
dc.contributor.departmentFarmacología
dc.contributor.otherFacultades de la UMU::Facultad de Medicina
dc.date.accessioned2026-02-02T11:12:52Z
dc.date.available2026-02-02T11:12:52Z
dc.date.copyright© 2012 by The American Society for Pharmacology and Experimental Therapeutics
dc.date.issued2012-05-29
dc.description.abstractThe negative affective states of withdrawal involve the recruitment of brain and peripheral stress circuitry [e.g., noradrenergic activity, induction of the hypothalamo-pituitary-adrenocortical (HPA) axis, and the expression and activation of heat shock proteins (Hsps)]. The present study investigated the role of extracellular signal-regulated protein kinase (ERK) and β-adrenoceptor on the response of stress systems to morphine withdrawal by the administration of [amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitrile (SL327), a selective inhibitor of ERK activation, or propranolol (a β-adrenoceptor antagonist). Dependence on morphine was induced by a 7-day subcutaneous implantation of morphine pellets. Morphine withdrawal was precipitated on day 8 by the injection of naloxone (2 mg/kg s.c.). Plasma concentrations of adrenocorticotropin and corticosterone were determined by radioimmunoassay; noradrenaline (NA) turnover in left ventricle was determined by high-performance liquid chromatography; and catechol-O-methyl transferase (COMT) and Hsp27 expression and phosphorylation at Ser82 were determined by quantitative blot immunolabeling. Morphine-withdrawn rats showed an increase of NA turnover and COMT expression in parallel with an enhancement of adrenocorticotropin and plasma corticosterone concentrations. In addition, we observed an enhancement of Hsp27 expression and phosphorylation. Pretreatment with SL327 or propranolol significantly reduced morphine withdrawal-induced increases of plasma adrenocorticotropin and Hsp27 phosphorylation at Ser82 without any changes in plasma corticosterone levels. The present findings demonstrate that morphine withdrawal is capable of inducing the activation of HPA axis in parallel with an enhancement of Hsp27 expression and Hsp27 phosphorylation at Ser82 and suggest a role for β-adrenoceptors and ERK pathways in mediating morphine-withdrawal activation of the HPA axis and cellular stress response.
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dc.identifier.citationThe Journal of Pharmacology and Experimental Therapeutics, 2012, Vol. 342, Issue 3, pp. 665-675
dc.identifier.doihttps://doi.org/10.1124/jpet.112.193581
dc.identifier.eissn1521-0103
dc.identifier.issn0022-3565
dc.identifier.urihttp://hdl.handle.net/10201/198069
dc.languageeng
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics (ASPET)
dc.relationThis work was supported by the Ministerio de Ciencia e Innovación [Grants SAF/FEDER (El Fondo Europeo de Desarrollo Regional) 2009-07178, 2010-17907]; and Red de Trastornos Adictivos [Grant RD06/0001/1006].
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/abs/pii/S0022356524183310
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleMorphine withdrawal activates hypothalamic-pituitary-adrenal axis and heat shock protein 27 in the left ventricle: the role of extracellular signal-regulated kinase
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublicationes
relation.isAuthorOfPublication5028b798-617b-4311-8389-11b8f71ac210
relation.isAuthorOfPublication19449ee0-5472-4d83-952f-8c9057f45b7c
relation.isAuthorOfPublication3563e5e9-0816-46a5-be3d-af02c0458d91
relation.isAuthorOfPublication.latestForDiscovery5028b798-617b-4311-8389-11b8f71ac210
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