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Chronic ethanol intake induces partial microglial activation that is not reversed by long-term ethanol withdrawal in the rat hippocampal formation

2017-05Journal article Restricted access
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dc.contributor.authorCruz, Catarina
dc.contributor.authorMeireles, Manuela
dc.contributor.authorSilva, Susana M.
dc.date.accessioned2019-11-20T15:07:37Z
dc.date.available2019-11-20T15:07:37Z
dc.date.issued2017-05
dc.description.abstractNeuroinflammation has been implicated in the pathogenesis of several disorders. Activation of microglia leads to the release of pro-inflammatory mediators and microglial-mediated neuroinflammation has been proposed as one of the alcohol-induced neuropathological mechanisms. The present study aimed to examine the effect of chronic ethanol exposure and long-term withdrawal on microglial activation and neuroinflammation in the hippocampal formation. Male rats were submitted to 6 months of ethanol treatment followed by a 2-month withdrawal period. Stereological methods were applied to estimate the total number of microglia and activated microglia detected by CD11b immunohistochemistry in the hippocampal formation. The expression levels of the pro-inflammatory cytokines TNF-alpha, COX-2 and IL-15 were measured by qRT-PCR. Alcohol consumption was associated with an increase in the total number of activated microglia but morphological assessment indicated that microglia did not exhibit a full activation phenotype. These data were supported by functional evidence since chronic alcohol consumption produced no changes in the expression of TNF-alpha or COX-2. The levels of IL-15 a cytokine whose expression is increased upon activation of both astrocytes and microglia, was induced by chronic alcohol treatment. Importantly, the partial activation of microglia induced by ethanol was not reversed by long-term withdrawal. This study suggests that chronic alcohol exposure induces a microglial phenotype consistent with partial activation without significant increase in classical cytokine markers of neuroinflammation in the hippocampal formation. Furthermore, long-term cessation of alcohol intake is not sufficient to alter the microglial partial activation phenotype induced by ethanol. (C) 2017 Elsevier B.V. All rights reserved.
dc.description.sponsorshipFCT - Fundacao para a Ciencia e a Tecnologia [UID/IC/4255/2013]
dc.description.versioninfo:eu-repo/semantics/publishedVersion
dc.identifier.doi10.1016/j.neuro.2017.04.005
dc.identifier.issn0161-813X
dc.identifier.issn1872-9711
dc.identifier.urihttp://hdl.handle.net/10400.1/13134
dc.language.isoeng
dc.peerreviewedyes
dc.publisherElsevier Science Bv
dc.subjectChronic alcohol-consumption
dc.subjectMessenger-Rna levels
dc.subjectNerve growth-factor
dc.subjectCell-death
dc.subjectInduced neuroinflammation
dc.subjectParaventricular nucleus
dc.subjectBrain-damage
dc.subjectIntake leads
dc.subjectNeurons
dc.subjectAstrocytes
dc.titleChronic ethanol intake induces partial microglial activation that is not reversed by long-term ethanol withdrawal in the rat hippocampal formation
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FIC%2F04255%2F2013/PT
oaire.citation.endPage115
oaire.citation.startPage107
oaire.citation.titleNeurotoxicology
oaire.citation.volume60
oaire.fundingStream5876
person.familyNameMeireles
person.givenNameManuela
person.identifier.orcid0000-0003-3703-0011
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsrestrictedAccess
rcaap.typearticle
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relation.isAuthorOfPublication.latestForDiscovery9f6adc84-c268-4bba-b03c-2c30de51fc27
relation.isProjectOfPublication5bbb0e3b-07ad-45f3-b0c8-6798efb2809d
relation.isProjectOfPublication.latestForDiscovery5bbb0e3b-07ad-45f3-b0c8-6798efb2809d

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