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Long-term inhibition of ethanol intake by the administration of an aldehyde dehydrogenase-2 (ALDH2)-coding lentiviral vector into the ventral tegmental area of rats

dc.contributor.authorKarahanian E.
dc.contributor.authorRivera-Meza M.
dc.contributor.authorTampier L.
dc.contributor.authorQuintanilla M.E.
dc.contributor.authorHerrera-Marschitz M.
dc.contributor.authorIsrael Y.
dc.date.accessioned2020-09-02T22:21:04Z
dc.date.available2020-09-02T22:21:04Z
dc.date.issued2015
dc.identifier10.1111/adb.12130
dc.identifier.citation20, 2, 336-344
dc.identifier.issn13556215
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4996
dc.descriptionPrevious studies suggest that acetaldehyde generated from ethanol in the brain is reinforcing. The present studies tested the feasibility of achieving a long-term reduction of chronic and post-deprivation binge ethanol drinking by a single administration into the brain ventral tegmental area (VTA) of a lentiviral vector that codes for aldehyde dehydrogenase-2 (ALDH2), which degrades acetaldehyde. The ALDH2 gene coding vector or a control lentiviral vector were microinjected into the VTA of rats bred for their alcohol preference. In the chronic alcohol administration model, naïve animals administered the control vector and subsequently offered 10% ethanol and water ingested 8-9-g ethanol/kg body weight/day. The single administration of the ALDH2-coding vector prior to allowing ethanol availability reduced ethanol drinking by 85-90% (P-<-0.001) for the 45 days tested. In the post-deprivation binge-drinking model, animals that had previously consumed ethanol chronically for 81 days were administered the lentiviral vector and were thereafter deprived of ethanol for three 7-day periods, each interrupted by a single 60-minute ethanol re-access after the last day of each deprivation period. Upon ethanol re-access, control vector-treated animals consumed intoxicating 'binge' amounts of ethanol, reaching intakes of 2.7-g ethanol/kg body weight in 60 minutes. The administration of the ALDH2-coding vector reduced re-access binge drinking by 75-80% (P-<-0.001). This study shows that endowing the ventral tegmental with an increased ability to degrade acetaldehyde greatly reduces chronic alcohol consumption and post-deprivation binge drinking for prolonged periods and supports the hypothesis that brain-generated acetaldehyde promotes alcohol drinking. © 2014 Society for the Study of Addiction.
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.subjectAcetaldehyde
dc.subjectADE
dc.subjectchronic ethanol intake
dc.subjectlentiviral vector
dc.subjectVTA
dc.subjectacetaldehyde
dc.subjectaldehyde dehydrogenase isoenzyme 2
dc.subjectlentivirus vector
dc.subjectaldehyde dehydrogenase
dc.subjectAldh2 protein, rat
dc.subjectmitochondrial protein
dc.subjectalcohol consumption
dc.subjectalcohol withdrawal
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectbinge drinking
dc.subjectcomparative study
dc.subjectcontrolled study
dc.subjectdrinking behavior
dc.subjectenzyme activity
dc.subjectgenetic code
dc.subjectHEK293 cell line
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectrat
dc.subjectventral tegmentum
dc.subjectalcoholism
dc.subjectanimal
dc.subjectdrug seeking behavior
dc.subjectgene vector
dc.subjectgenetics
dc.subjectLentivirinae
dc.subjectmetabolism
dc.subjectreinforcement
dc.subjectventral tegmentum
dc.subjectAcetaldehyde
dc.subjectAlcohol Drinking
dc.subjectAlcoholism
dc.subjectAldehyde Dehydrogenase
dc.subjectAnimals
dc.subjectBinge Drinking
dc.subjectDrug-Seeking Behavior
dc.subjectGenetic Vectors
dc.subjectLentivirus
dc.subjectMitochondrial Proteins
dc.subjectRats
dc.subjectReinforcement (Psychology)
dc.subjectVentral Tegmental Area
dc.titleLong-term inhibition of ethanol intake by the administration of an aldehyde dehydrogenase-2 (ALDH2)-coding lentiviral vector into the ventral tegmental area of rats
dc.typeArticle


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