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dc.contributor.authorMartín, Fátima
dc.contributor.authorNúñez, Cristina
dc.contributor.authorMarín Boscá, María Teresa
dc.contributor.authorLaorden, María Luisa
dc.contributor.authorKovács, Krisztina J.
dc.contributor.authorMilanés, M. Victoria
dc.date.accessioned2014-03-24T10:29:57Z
dc.date.available2014-03-24T10:29:57Z
dc.date.issued2012
dc.identifier.citationMartín, F.; et al. Involvement of Noradrenergic Transmission in the PVN on CREB Activation, TORC1 Levels, and Pituitary-Adrenal Axis Activity during Morphine Withdrawal. Plos One, 7(2): e31119 (2012). [http://hdl.handle.net/10481/31059]es_ES
dc.identifier.issn1932-6203
dc.identifier.otherdoi: 10.1371/journal.pone.0031119
dc.identifier.urihttp://hdl.handle.net/10481/31059
dc.description.abstractExperimental and clinical findings have shown that administration of adrenoceptor antagonists alleviated different aspects of drug withdrawal and dependence. The present study tested the hypothesis that changes in CREB activation and phosphorylated TORC1 levels in the hypothalamic paraventricular nucleus (PVN) after naloxone-precipitated morphine withdrawal as well as the HPA axis activity arises from α1- and/or β-adrenoceptor activation. The effects of morphine dependence and withdrawal on CREB phosphorylation (pCREB), phosphorylated TORC1 (pTORC1), and HPA axis response were measured by Western-blot, immunohistochemistry and radioimmunoassay in rats pretreated with prazosin (α1-adrenoceptor antagonist) or propranolol (β-adrenoceptor antagonist). In addition, the effects of morphine withdrawal on MHPG (the main NA metabolite at the central nervous system) and NA content and turnover were evaluated by HPLC. We found an increase in MHPG and NA turnover in morphine-withdrawn rats, which were accompanied by increased pCREB immunoreactivity and plasma corticosterone concentrations. Levels of the inactive form of TORC1 (pTORC1) were decreased during withdrawal. Prazosin but not propranolol blocked the rise in pCREB level and the decrease in pTORC1 immunoreactivity. In addition, the HPA axis response to morphine withdrawal was attenuated in prazosin-pretreated rats. Present results suggest that, during acute morphine withdrawal, NA may control the HPA axis activity through CREB activation at the PVN level. We concluded that the combined increase in CREB phosphorylation and decrease in pTORC1 levels might represent, in part, two of the mechanisms of CREB activation at the PVN during morphine withdrawal.es_ES
dc.description.sponsorshipThis work was supported by Ministerio de Ciencia e Innovación (SAF2009-07178 and SAF2010-17907), Red de Trastornos Adictivos (RTA; RD06/0001/1006) and Fundación Séneca (15405/PI/10), Agencia Regional de Ciencia y Tecnología, Región de Murcia.es_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Science (PLOS)es_ES
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs 3.0 Licensees_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es_ES
dc.subjectAnalysis of variance es_ES
dc.subjectBody weightes_ES
dc.subjectDNA transcriptiones_ES
dc.subjectDrug addictiones_ES
dc.subjectMorphine es_ES
dc.subjectNeurons es_ES
dc.subjectOpiateses_ES
dc.subjectPhosphorylationes_ES
dc.titleInvolvement of Noradrenergic Transmission in the PVN on CREB Activation, TORC1 Levels, and Pituitary-Adrenal Axis Activity during Morphine Withdrawales_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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