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dc.rights.licenseopenen_US
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorCAPURON, Lucile
IDREF: 167018736
hal.structure.identifierUniversità degli Studi di Modena e Reggio Emilia = University of Modena and Reggio Emilia [UNIMORE]
dc.contributor.authorPAGNONI, Giuseppe
dc.contributor.authorDRAKE, Daniel F
dc.contributor.authorWOOLWINE, Bobbi J
hal.structure.identifierEmory University School of Medicine
dc.contributor.authorSPIVEY, James R
hal.structure.identifierEmory University School of Medicine
dc.contributor.authorCROWE, Ronald J
hal.structure.identifierEmory University School of Medicine
dc.contributor.authorVOTAW, John R
hal.structure.identifierEmory University School of Medicine
dc.contributor.authorGOODMAN, Mark M
hal.structure.identifierEmory University School of Medicine
dc.contributor.authorMILLER, Andrew H
dc.date.accessioned2022-03-23T15:09:00Z
dc.date.available2022-03-23T15:09:00Z
dc.date.issued2012-10-01
dc.identifier.issn1538-3636en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/136521
dc.description.abstractEnInflammatory cytokines or cytokine inducers can alter basal ganglia activity, including reducing responsiveness to rewarding stimuli that may be mediated by cytokine effects on dopamine function. To determine whether long-term administration of the inflammatory cytokine interferon alfa reduces the basal ganglia response to reward and whether such changes are associated with decreased presynaptic striatal dopamine function and altered behavior. Cross-sectional and longitudinal studies. Outpatient research unit and neuroimaging facilities at Emory University, Atlanta, Georgia. Medically stable adults with chronic hepatitis C virus (HCV) infection eligible for interferon alfa treatment. Neural activity in the ventral striatum during a hedonic reward task as measured by functional magnetic resonance imaging, uptake and turnover of radiolabeled fluorodopa F 18 (18F-dopa) in caudate and putamen using positron emission tomography, and interferon alfa-induced depression, anhedonia, fatigue, and neurotoxicity. Patients with HCV receiving interferon alfa for 4 to 6 weeks (n = 14) exhibited significantly reduced bilateral activation of the ventral striatum in the win vs lose condition of a gambling task compared with patients with HCV awaiting interferon alfa treatment (n = 14). Reduced activation of the ventral striatum was, in turn, significantly correlated with anhedonia, depression, and fatigue. In a separate longitudinal study, patients with HCV treated with interferon alfa for 4 to 6 weeks (n = 12) exhibited significantly increased 18F-dopa uptake and decreased 18F-dopa turnover in caudate and putamen and in the same ventral striatal regions identified in the functional magnetic resonance imaging study. Baseline and percentage change in 18F-dopa uptake and turnover were correlated with behavioral alterations, including depression, fatigue, and neurotoxicity, during interferon alfa administration. These data replicate and extend findings that inflammatory stimuli, including inflammatory cytokines, such as interferon alfa, alter basal ganglia activity and behavior in association with significant changes in presynaptic striatal dopamine function consistent with decreased dopamine synthesis or release.
dc.language.isoENen_US
dc.subject.enAdult
dc.subject.enCorpus Striatum
dc.subject.enDihydroxyphenylalanine
dc.subject.enDopamine
dc.subject.enFemale
dc.subject.enHepatitis C
dc.subject.enChronic
dc.subject.enHumans
dc.subject.enInterferon-alpha
dc.subject.enMagnetic Resonance Imaging
dc.subject.enMale
dc.subject.enMental Disorders
dc.subject.enMiddle Aged
dc.subject.enNeuropsychological Tests
dc.subject.enPositron-Emission Tomography
dc.subject.enReward
dc.title.enDopaminergic mechanisms of reduced basal ganglia responses to hedonic reward during interferon alfa administration.
dc.title.alternativeArch Gen Psychiatryen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1001/archgenpsychiatry.2011.2094en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed23026954en_US
bordeaux.journalArchives of General Psychiatryen_US
bordeaux.page1044-53en_US
bordeaux.volume69en_US
bordeaux.hal.laboratoriesNutriNeurO (Laboratoire de Nutrition et Neurobiologie Intégrée) - UMR 1286en_US
bordeaux.issue10en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINRAEen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.exportfalse
workflow.import.sourcepubmed
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Archives%20of%20General%20Psychiatry&rft.date=2012-10-01&rft.volume=69&rft.issue=10&rft.spage=1044-53&rft.epage=1044-53&rft.eissn=1538-3636&rft.issn=1538-3636&rft.au=CAPURON,%20Lucile&PAGNONI,%20Giuseppe&DRAKE,%20Daniel%20F&WOOLWINE,%20Bobbi%20J&SPIVEY,%20James%20R&rft.genre=article


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