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Ethanol exposure selectively alters beta-endorphin content but not [H-3]-DAMGO binding in discrete regions of the rat brain

dc.creatorLeriche, M.
dc.creatorMéndez, M.
dc.date.accessioned2017-06-30T03:56:34Z
dc.date.available2017-06-30T03:56:34Z
dc.date.issued2010es_ES
dc.identifier2397es_ES
dc.identifier.issn0143-4179es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7040
dc.identifier.urihttps://doi.org/10.1016/j.npep.2009.11.009es_ES
dc.language.isoenges_ES
dc.publisherChurchill Livingstone, Journal Production Dept, Robert Stevenson House, 1-3 Baxters Place, Leith Walk, Edinburgh EH1 3AF, Midlothian, Scotlandes_ES
dc.relation44 (1) 9-16 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleEthanol exposure selectively alters beta-endorphin content but not [H-3]-DAMGO binding in discrete regions of the rat braines_ES
dc.typearticlees_ES
dc.contributor.affiliationInst Nacl Psiquiatria Ramon Fuente, Dept Neuroquim, Subdirecc Invest Clin, Calzada Mexico Xochimilco 101,Col San Lorenzo Hui, Mexico City 14370, DF, Mexico.es_ES
dc.contributor.emailubach@imp.edu.mxes_ES
dc.relation.jnabreviadoNEUROPEPTIDESes_ES
dc.relation.journalNeuropeptideses_ES
dc.identifier.placeMidlothianes_ES
dc.date.published2010es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México.es_ES
dc.identifier.eissn1532-2785es_ES
dc.identifier.doi10.1016/j.npep.2009.11.009es_ES
dc.description.monthFebes_ES
dc.description.abstractotrodiomaThe dopaminergic mesocorticolimbic system plays an important role in the reinforcing effects of ethanol. Opioid peptides modulate the activity of this system and have been suggested to mediate, at least in part, the reinforcing properties of ethanol. Thus, beta-endorphin (beta-END) could participate in the development of ethanol reinforcement and addiction. The aim of this work was to investigate the acute and chronic ethanol effects on beta-END content in regions of the mesolimbic system and to examine if chronic ethanol treatment alters ligand binding to mu opioid receptor (mu OR). Male Wistar rats received a single acute ethanol dose of 2.5 g/kg or water by intra-gastric administration. For chronic ethanol treatment experiments, one group of rats was given ethanol (10% v/v solution) to drink, two groups were given equivalent volume of sucrose (14.14% isocaloric solution) or water, respectively, and a fourth group had ad libitum access to food and water. Treatment was followed for 4 weeks. Beta-endorphin content in brain regions was quantified by radioimmunoassay and ligand binding Studies to mu OR were performed by quantitative autoradiography using 8 nM [H-3]-DAMGO as radioligand. Acute ethanol decreased beta-END content in the hypothalamus (26%) 1 h after administration. No ethanol effects were observed in the midbrain, ventral tegmental area, substantia nigra, nucleus accumbens, nucleus accumbens-septum and prefrontal cortex. Chronic ethanol treatment neither changed beta-END levels nor [H-3]-DAMGO binding to mu opioid receptors in any of the regions Studied. However, beta-END levels in the Sucrose group were significantly increased in the nucleus accumbens and substantia nigra, in comparison to all other groups. These findings suggest that different neural mechanisms and specific brain regions may be involved in the reinforcing effects of ethanol and Sucrose. (C) 2009 Elsevier Ltd. All rights reserved.es_ES
dc.subject.kwEtanoles_ES
dc.subject.kwPéptidos opioideses_ES
dc.subject.kwB-endorfinaes_ES
dc.subject.kwReceptor de opioides Mues_ES
dc.subject.kwSistema dopaminérgico mesocorticolímbicoes_ES
dc.subject.kwHipotálamoes_ES
dc.subject.kwSacarosaes_ES
dc.subject.koEthanoles_ES
dc.subject.koOpioid peptideses_ES
dc.subject.koB-Endorphines_ES
dc.subject.koMu opioid receptores_ES
dc.subject.koDopaminergic mesocorticolimbic systemes_ES
dc.subject.koHypothalamuses_ES
dc.subject.koSucrosees_ES


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