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• W2953358724 abstract "BackgroundNaltrexone is a nonselective opioid receptor antagonist used as a treatment for alcohol use disorder. However, only modest clinical effects have been observed, possibly because of limited knowledge about the biological variables affecting the efficacy of naltrexone. We investigated the potential role of the kappa opioid receptor (KOR) in the therapeutic effect of naltrexone.MethodsA total of 48 non-treatment-seeking heavy drinkers (16 women) who met DSM-IV criteria for alcohol dependence participated in two alcohol drinking paradigms (ADPs) separated by a week of open-label naltrexone (100 mg daily). Craving, assessed with the Alcohol Urge Questionnaire and the Yale Craving Scale, and drinking behavior were recorded in each ADP. Prior to naltrexone initiation, KOR availability was determined in the amygdala, hippocampus, pallidum, striatum, cingulate cortex, and prefrontal cortex using positron emission tomography with [11C]LY2795050.ResultsParticipants reported lower levels of craving (Yale Craving Scale: −11 ± 1, p < .0001; Alcohol Urge Questionnaire: −6 ± 0.6, p < .0001) and consumed fewer drinks (−3.7 ± 4, p < .0001) during the second ADP following naltrexone therapy. The observed reduction in drinking was negatively associated with baseline KOR availability in the striatum (p = .005), pallidum (p = .023), and cingulate cortex (p = .018). Voxelwise analysis identified clusters in the bilateral insula, prefrontal, and cingulate cortex associated with the reduction in drinking (p < .0001). In addition, KOR availability in all evaluated brain regions was associated with craving measured in both ADPs.ConclusionsThe KOR is implicated in drinking and craving following naltrexone therapy in alcohol use disorder." @default.
• W2953358724 created "2019-06-27" @default.
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• W2953358724 date "2019-12-01" @default.
• W2953358724 modified "2023-09-27" @default.
• W2953358724 title "The Kappa Opioid Receptor Is Associated With Naltrexone-Induced Reduction of Drinking and Craving" @default.
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• W2953358724 doi "https://doi.org/10.1016/j.biopsych.2019.05.021" @default.
• W2953358724 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31399255" @default.
• W2953358724 hasPublicationYear "2019" @default.
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