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dc.contributor.authorMoreira-Silva, Daniel
dc.contributor.authorMorais-Silva, Gessynger
dc.contributor.authorFernandes-Santos, Juliana
dc.contributor.authorPlaneta, Cleopatra da Silva [UNESP]
dc.contributor.authorMarin, Marcelo Tadeu [UNESP]
dc.date.accessioned2014-12-03T13:09:00Z
dc.date.available2014-12-03T13:09:00Z
dc.date.issued2014-05-01
dc.identifierhttp://dx.doi.org/10.1111/acer.12388
dc.identifier.citationAlcoholism-clinical And Experimental Research. Hoboken: Wiley-blackwell, v. 38, n. 5, p. 1227-1236, 2014.
dc.identifier.issn0145-6008
dc.identifier.urihttp://hdl.handle.net/11449/111819
dc.description.abstractBackgroundConditioned place preference (CPP) to ethanol (EtOH) is an important addiction-related alteration thought to be mediated by changed neurotransmission in the mesocorticolimbic brain pathway. Stress is a factor of major importance for the initiation, maintenance, and reinstatement of drug abuse and modulates the neurochemical outcomes of drugs. Thus, the aim of this study was to investigate the effects of concomitant exposure to chronic EtOH and stress on CPP to this drug and alterations of dopaminergic and serotonergic neurotransmission in mice.MethodsMale Swiss mice were chronically treated with EtOH via a liquid diet and were exposed to forced swimming stress. After treatment, animals were evaluated for conditioning, extinction, and reinstatement of CPP to EtOH. Also, mice exposed to the same treatment protocol had their prefrontal cortex (PFC), nucleus accumbens (NAc), and amygdala dissected for the quantitation of dopamine, serotonin, and their metabolites content.ResultsData showed that previous chronic exposure to EtOH potentiated EtOH conditioning and increased dopaminergic turnover in PFC. Exposure to stress potentiated EtOH conditioning and decreased dopaminergic turnover in the NAc. However, animals exposed to both chronic EtOH and stress did not display alterations of CPP and showed an elevated content of dopamine in amygdala. No treatment yielded serotonergic changes.ConclusionsThe present study indicates that previous EtOH consumption as well as stress exposure induces increased EtOH conditioning, which can be related to dopaminergic alterations in the PFC or NAc. Interestingly, concomitant exposure to both stimuli abolished each other's effect on conditioning and PFC or NAc alterations. This protective outcome can be related to the dopaminergic increase in the amygdala.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)
dc.format.extent1227-1236
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofAlcoholism: Clinical and Experimental Research
dc.sourceWeb of Science
dc.subjectEthanolen
dc.subjectStressen
dc.subjectAddictionen
dc.subjectPlace Preferenceen
dc.subjectDopamineen
dc.titleStress Abolishes the Effect of Previous Chronic Ethanol Consumption on Drug Place Preference and on the Mesocorticolimbic Brain Pathwayen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderWiley-Blackwell
dc.contributor.institutionUniversidade Federal de Uberlândia (UFU)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationUniv Fed Uberlandia, Inst Biomed Sci, BR-38400 Uberlandia, MG, Brazil
dc.description.affiliationUniv Estadual Paulista UNESP, Sch Pharmaceut Sci, Pharmacol Lab, BR-14801902 Araraquara, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista UNESP, Sch Pharmaceut Sci, Pharmacol Lab, BR-14801902 Araraquara, SP, Brazil
dc.identifier.doi10.1111/acer.12388
dc.identifier.wosWOS:000334657200006
dc.rights.accessRightsAcesso restrito
dc.description.sponsorshipIdFAPEMIG: CBB-APQ-04545-10
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Ciências Farmacêuticas, Araraquarapt
dc.identifier.lattes2514762545280942
dc.identifier.lattes7920438802539727
dc.identifier.orcid0000-0002-1378-6327
unesp.author.lattes7920438802539727
unesp.author.lattes2514762545280942[4]
unesp.author.orcid0000-0002-0522-2839[5]
unesp.author.orcid0000-0002-8859-2826[1]
unesp.author.orcid0000-0002-1387-9881[2]
unesp.author.orcid0000-0002-1378-6327[4]
dc.relation.ispartofjcr3.183
dc.relation.ispartofsjr1,449
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