Different brain oxidative and neuroinflammation status in rats during prolonged abstinence depending on their ethanol relapse-like drinking behavior: Effects of ethanol reintroduction
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Different brain oxidative and neuroinflammation status in rats during prolonged abstinence depending on their ethanol relapse-like drinking behavior: Effects of ethanol reintroduction

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Different brain oxidative and neuroinflammation status in rats during prolonged abstinence depending on their ethanol relapse-like drinking behavior: Effects of ethanol reintroduction

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dc.contributor.author Fernández Rodríguez, Sandra
dc.contributor.author Cano Cebrián, María José
dc.contributor.author Rius Pérez, Sergio
dc.contributor.author Pérez Garrido, Salvador
dc.contributor.author Guerri Sirera, Consuelo
dc.contributor.author Granero Maciá, Luis
dc.contributor.author Zornoza Sabina, Teodoro
dc.contributor.author Polache Vengut, Ana
dc.date.accessioned 2022-02-09T15:08:57Z
dc.date.available 2022-02-09T15:08:57Z
dc.date.issued 2022
dc.identifier.uri https://hdl.handle.net/10550/81556
dc.description.abstract Rationale: Accumulating evidence suggests that chronic alcohol consumption is associated with excessive oxidative damage and neuroinflammatory processes and these events have been associated to early alcohol withdrawal. In the present research we wonder if brain oxidative stress and neuroinflammation remains altered during prolonged withdrawal situations and whether these alterations can be correlated with relapse behavior in alcohol consumption. The effects of alcohol reintroduction were also evaluated. Methods: We have used a model based on the alcohol deprivation effect (ADE) within a cohort of wild-type male Wistar rats. Two subpopulations were identified according to the alcohol relapse-like drinking behavior displayed (ADE and NO-ADE subpopulations). Oxidized and reduced glutathione content was determined within the hippocampus and the amygdala using a mass spectrometry method. The levels of mRNA of seven different inflammatory mediators in the prefrontal cortex of rats were quantified. All the analyses were performed in two different conditions: after 21-day alcohol deprivation (prolonged abstinence) and after 24 h of ethanol reintroduction in both subpopulations. Results: ADE and NO-ADE rats showed different endophenotypes. ADE rats always displayed a significant lower alcohol intake rate and ethanol preference than NO-ADE rats. The results also demonstrated the existence of altered brain redox and neuroinflammation status after prolonged abstinence exclusively in ADE rats. Moreover, when ethanol was reintroduced in the ADE subpopulation, altered oxidative stress and neuroinflammatory markers were restored. Conclusions: Present findings provide new mechanisms underlying the neurobiology of relapse behavior and suggest the development of new pharmacological approaches to treat alcohol-induced relapse.
dc.language.iso eng
dc.relation.ispartof Drug and Alcohol Dependence, 2022, vol. 232, p. 109284
dc.rights.uri info:eu-repo/semantics/openAccess
dc.source Fernández Rodríguez, Sandra Cano Cebrián, María José Rius Pérez, Sergio Pérez Garrido, Salvador Guerri Sirera, Consuelo Granero Maciá, Luis Zornoza Sabina, Teodoro Polache Vengut, Ana 2022 Different brain oxidative and neuroinflammation status in rats during prolonged abstinence depending on their ethanol relapse-like drinking behavior: Effects of ethanol reintroduction Drug and Alcohol Dependence 232 109284
dc.subject Estrès oxidatiu
dc.subject Alcohol Efectes fisiològics
dc.title Different brain oxidative and neuroinflammation status in rats during prolonged abstinence depending on their ethanol relapse-like drinking behavior: Effects of ethanol reintroduction
dc.type info:eu-repo/semantics/article
dc.date.updated 2022-02-09T15:08:57Z
dc.identifier.doi https://doi.org/10.1016/j.drugalcdep.2022.109284
dc.identifier.idgrec 150232

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