Bupropion, a possible antidepressant without negative effects on alcohol relapse

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dc.contributor.authorAlén Fariñas, Francisco
dc.contributor.authorGómez De Heras, María Raquel
dc.contributor.authorOrio Ortiz, Laura
dc.contributor.authorRodríguez De Fonseca, Fernando Antonio
dc.contributor.authorAntonio Ballesta
dc.contributor.authorRocío Arco
dc.contributor.authorAntonio Vargas
dc.contributor.authorPablo Romero-Sanchiz
dc.contributor.authorRaquel Nogueira-Arjona
dc.contributor.authorMaría Antón
dc.contributor.authorMayte Ramírez-López
dc.contributor.authorAntonia Serrano
dc.contributor.authorFrancisco Javier Pavón
dc.contributor.authorJuan Suárez
dc.date.accessioned2024-02-12T16:42:19Z
dc.date.available2024-02-12T16:42:19Z
dc.date.issued2019-06-12
dc.description.abstractRationale: the role that antidepressants play on alcohol consumption is not well understood. Previous studies have reported that treatment with a Selective Serotonin Reuptake Inhibitor (SSRIs) increases alcohol consumption in an animal model of relapse, however it is unknown whether this effect holds for other antidepressants such as the atypical dopamine/norepinephrine reuptake inhibitors (SNDRI). Objectives: the main goal of the present study was to compare the effects of two classes of antidepressants drugs, bupropion (SNDRI) and fluoxetine (SSRI), on alcohol consumption during relapse. Since glutamatergic and endocannabinoid signaling systems plays an important rolein alcohol abuse and relapse, we also evaluated the effects of both antidepressants ontheexpression of the main important genes and proteins of both systems in the prefrontal cortex,a critical brain region in alcohol relapse. Methods: rats were trained to self-administered alcohol. During abstinence, rats received a14d-treatment with vehicle, fluoxetine (10 mg/kg) or bupropion (20 mg/kg), and we evaluatedalcohol consumption during relapse for 3 weeks. Samples of prefrontal cortex were taken toevaluate the mRNA and protein expression of the different components of glutamatergic andendocannabinoid signaling systems. Results: fluoxetine treatment induced a long-lasting increase in alcohol consumption during relapse, an effect that was not observed in the case of bupropion treatment. The observed increases in alcohol consumption were accompanied by distinct alterations in the glutamate and endocannabinoid systems. Conclusions: our results suggest that SSRIs can negatively impact alcohol consumption in relapse while SNDRIs have no effects. The observed increase in alcohol consumption are accompanied by functional alterations in the glutamatergic and endocannabinoid systems. This finding could open new strategies for the treatment of depression in patients with alcohol use disorders.
dc.description.departmentDepto. de Psicobiología y Metodología en Ciencias del Comportamiento
dc.description.facultyFac. de Psicología
dc.description.refereedTRUE
dc.description.statuspub
dc.identifier.doi10.1016/j.euroneuro.2019.03.012
dc.identifier.issn0924-977X
dc.identifier.officialurlhttps://doi.org/10.1016/j.euroneuro.2019.03.012
dc.identifier.relatedurlhttps://www.sciencedirect.com/science/article/pii/S0924977X19302007?via%3Dihub
dc.identifier.urihttps://hdl.handle.net/20.500.14352/101311
dc.journal.titleEuropean Neuropsychopharmacology
dc.language.isoeng
dc.page.final765
dc.page.initial756
dc.rights.accessRightsrestricted access
dc.subject.keywordAlcohol
dc.subject.keywordPrefrontal cortex
dc.subject.keywordAntidepressant
dc.subject.keywordCannabinoid
dc.subject.keywordGlutamate
dc.subject.keywordRelapse
dc.subject.ucmPsicofarmacología
dc.subject.unesco6113 Psicofarmacología
dc.titleBupropion, a possible antidepressant without negative effects on alcohol relapse
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number29
dspace.entity.typePublication
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relation.isAuthorOfPublicationfca2f268-62c3-41a8-ac34-25666f7e2a56
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