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The "first hit" toward alcohol reinforcement: Role of ethanol metabolites

dc.contributor.authorIsrael Y.
dc.contributor.authorQuintanilla M.E.
dc.contributor.authorKarahanian E.
dc.contributor.authorRivera-Meza M.
dc.contributor.authorHerrera-Marschitz M.
dc.date.accessioned2020-09-02T22:20:39Z
dc.date.available2020-09-02T22:20:39Z
dc.date.issued2015
dc.identifier10.1111/acer.12709
dc.identifier.citation39, 5, 776-786
dc.identifier.issn01456008
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4954
dc.descriptionThis review analyzes literature that describes the behavioral effects of 2 metabolites of ethanol (EtOH): acetaldehyde and salsolinol (a condensation product of acetaldehyde and dopamine) generated in the brain. These metabolites are self-administered into specific brain areas by animals, showing strong reinforcing effects. A wealth of evidence shows that EtOH, a drug consumed to attain millimolar concentrations, generates brain metabolites that are reinforcing at micromolar and nanomolar concentrations. Salsolinol administration leads to marked increases in voluntary EtOH intake, an effect inhibited by mu-opioid receptor blockers. In animals that have ingested EtOH chronically, the maintenance of alcohol intake is no longer influenced by EtOH metabolites, as intake is taken over by other brain systems. However, after EtOH withdrawal brain acetaldehyde has a major role in promoting binge-like drinking in the condition known as the "alcohol deprivation effect" a condition seen in animals that have ingested alcohol chronically, are deprived of EtOH for extended periods, and are allowed EtOH re-access. The review also analyzes the behavioral effects of acetate, a metabolite that enters the brain and is responsible for motor incoordination at low doses of EtOH. Also discussed are the paradoxical effects of systemic acetaldehyde. Overall, evidence strongly suggests that brain-generated EtOH metabolites play a major role in the early ("first-hit") development of alcohol reinforcement and in the generation of relapse-like drinking. © 2015 by the Research Society on Alcoholism.
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.subjectAcetaldehyde
dc.subjectAcetate
dc.subjectAlcohol deprivation effect
dc.subjectReinforcement
dc.subjectSalsolinol
dc.subjectSelf-administration
dc.subjectacetaldehyde
dc.subjectacetic acid
dc.subjectalcohol
dc.subjectmu opiate receptor antagonist
dc.subjectsalsolinol
dc.subjectacetaldehyde
dc.subjectacetic acid derivative
dc.subjectalcohol
dc.subjectisoquinoline derivative
dc.subjectsalsolinol
dc.subjectalcohol blood level
dc.subjectalcohol consumption
dc.subjectalcohol metabolism
dc.subjectanimal behavior
dc.subjectbinge drinking
dc.subjectblood brain barrier
dc.subjectbrain metabolism
dc.subjectcerebrospinal fluid
dc.subjectmotor coordination
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectReview
dc.subjectanimal
dc.subjectbrain
dc.subjectdrug effects
dc.subjectdrug seeking behavior
dc.subjectdrug self administration
dc.subjectmetabolism
dc.subjectreinforcement
dc.subjectAnimalia
dc.subjectAcetaldehyde
dc.subjectAcetates
dc.subjectAnimals
dc.subjectBrain
dc.subjectDrug-Seeking Behavior
dc.subjectEthanol
dc.subjectIsoquinolines
dc.subjectReinforcement (Psychology)
dc.subjectSelf Administration
dc.titleThe "first hit" toward alcohol reinforcement: Role of ethanol metabolites
dc.typeReview


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