Acquisition, maintenance and relapse-like alcohol drinking: lessons from the UChB rat line

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dc.contributor.authorIsrael, Yedy
dc.contributor.authorKarahanian, Eduardo
dc.contributor.authorEzquer, Fernando
dc.contributor.authorMorales, Paola
dc.contributor.authorEzquer, Marcelo
dc.contributor.authorRivera-Meza, Mario
dc.contributor.authorHerrera-Marschitz, Mario
dc.contributor.authorQuintanilla, Maria E
dc.date.accessioned2017-10-02T14:51:21Z
dc.date.available2017-10-02T14:51:21Z
dc.date.issued2017
dc.description.abstractThis review article addresses the biological factors that influence: (i) the acquisition of alcohol intake; (ii) the maintenance of chronic alcohol intake; and (iii) alcohol relapse-like drinking behavior in animals bred for their high-ethanol intake. Data from several rat strains/lines strongly suggest that catalase-mediated brain oxidation of ethanol into acetaldehyde is an absolute requirement (up 80%-95%) for rats to display ethanol's reinforcing effects and to initiate chronic ethanol intake. Acetaldehyde binds non-enzymatically to dopamine forming salsolinol, a compound that is self-administered. In UChB rats, salsolinol: (a) generates marked sensitization to the motivational effects of ethanol; and (b) strongly promotes binge-like drinking. The specificity of salsolinol actions is shown by the finding that only the R-salsolinol enantiomer but not S-salsolinol accounted for the latter effects. Inhibition of brain acetaldehyde synthesis does not influence the maintenance of chronic ethanol intake. However, a prolonged ethanol withdrawal partly returns the requirement for acetaldehyde synthesis/levels both on chronic ethanol intake and on alcohol relapse-like drinking. Chronic ethanol intake, involving the action of lipopolysaccharide diffusing from the gut, and likely oxygen radical generated upon catechol/salsolinol oxidation, leads to oxidative stress and neuro-inflammation, known to potentiate each other. Data show that the administration of N-acetyl cysteine (NAC) a strong antioxidant inhibits chronic ethanol maintenance by 60%-70%, without inhibiting its initial intake. Intra-cerebroventricular administration of mesenchymal stem cells (MSCs), known to release anti-inflammatory cytokines, to elevate superoxide dismutase levels and to reverse ethanol-induced hippocampal injury and cognitive deficits, also inhibited chronic ethanol maintenance; further, relapse-like ethanol drinking was inhibited up to 85% for 40 days following intracerebral stem cell administration. Thus: (i) ethanol must be metabolized intracerebrally into acetaldehyde, and further into salsolinol, which appear responsible for promoting the acquisition of the early reinforcing effects of ethanol; (ii) acetaldehyde is not responsible for the maintenance of chronic ethanol intake, while other mechanisms are indicated; (iii) the systemic administration of NAC, a strong antioxidant markedly inhibits the maintenance of chronic ethanol intake; and (iv) the intra-cerebroventricular administration of anti-inflammatory and antioxidant MSCs inhibit both the maintenance of chronic ethanol intake and relapse-like drinking.
dc.format.extent15
dc.identifier.citationIsrael Y, Karahanian E, Ezquer F, Morales P, Ezquer M, Rivera-Meza M, Herrera-Marschitz M, Quintanilla ME. Acquisition, Maintenance and Relapse-Like Alcohol Drinking: Lessons from the UChB Rat Line. Front Behav Neurosci. 2017 Apr 4;11:57
dc.identifier.urihttp://hdl.handle.net/11447/1683
dc.identifier.urihttp://dx.doi.org/10.3389/fnbeh.2017.00057
dc.language.isoen_US
dc.publisherFrontiers Research Foundation
dc.subjectAcetaldehyde
dc.subjectCatalase
dc.subjectEthanol
dc.subjectInflammation
dc.subjectReactive oxygen species (ROS)
dc.subjectReinforcement (psychology)
dc.subjectRelapse
dc.subjectStem cells
dc.titleAcquisition, maintenance and relapse-like alcohol drinking: lessons from the UChB rat line
dc.typeArtículo

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