Karmen K Yoder1, Daniel S Albrecht2, Mario Dzemidzic3, Marc D Normandin4, Lauren M Federici5, Tammy Graves6, Christine M Herring5, Karen L Hile5, James W Walters5, Tiebing Liang7, Martin H Plawecki8, Sean O'Connor9, David A Kareken10. 1. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA; Center for Neuroimaging, IUSM, GH Ste. 4100, 355 W. 16th St., Indianapolis, IN 46202, USA; Stark Neurosciences Research Institute, IUSM, NB Ste. 414, 320 W. 16th St., Indianapolis, IN 46202, USA; Department of Psychology, Indiana University-Purdue University at Indianapolis, 402 N. Blackford St., Indianapolis, IN 46202, USA. Electronic address: kkyoder@iupui.edu. 2. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA; Center for Neuroimaging, IUSM, GH Ste. 4100, 355 W. 16th St., Indianapolis, IN 46202, USA; Stark Neurosciences Research Institute, IUSM, NB Ste. 414, 320 W. 16th St., Indianapolis, IN 46202, USA. 3. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA; Center for Neuroimaging, IUSM, GH Ste. 4100, 355 W. 16th St., Indianapolis, IN 46202, USA; Department of Neurology, IUSM, GH Ste. 4700, 355 W. 16th St., Indianapolis, IN 46202, USA. 4. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA. 5. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA; Center for Neuroimaging, IUSM, GH Ste. 4100, 355 W. 16th St., Indianapolis, IN 46202, USA. 6. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA; Department of Medicine, IUSM, 340 W. 10th St., Ste. 6200, Indianapolis, IN 46202, USA. 7. Department of Medicine, IUSM, 340 W. 10th St., Ste. 6200, Indianapolis, IN 46202, USA. 8. Department of Psychiatry, IUSM, GH Ste. 4800, 355 W. 16th St., Indianapolis, IN 46202, USA. 9. Department of Psychiatry, IUSM, GH Ste. 4800, 355 W. 16th St., Indianapolis, IN 46202, USA; Roudebush Veteran's Administration Medical Center, 1481 W. 10th St., Indianapolis, IN 46202, USA. 10. Department of Radiology and Imaging Sciences, Indiana University School of Medicine (IUSM), R2-E124, 950 W. Walnut St., Indianapolis, IN, USA; Center for Neuroimaging, IUSM, GH Ste. 4100, 355 W. 16th St., Indianapolis, IN 46202, USA; Department of Neurology, IUSM, GH Ste. 4700, 355 W. 16th St., Indianapolis, IN 46202, USA; Department of Psychiatry, IUSM, GH Ste. 4800, 355 W. 16th St., Indianapolis, IN 46202, USA.
Abstract
BACKGROUND: Striatal dopamine (DA) has been implicated in alcohol use disorders, but it is still unclear whether or not alcohol can induce dopamine release in social drinkers. Furthermore, no data exist on dopamine responses to alcohol in dependent drinkers. We sought to characterize the DA responses to alcohol intoxication in moderately large samples of social drinkers (SD) and nontreatment-seeking alcoholics (NTS). METHODS: Twenty-four SD and twenty-one NTS received two [(11)C]raclopride (RAC) PET scans; one at rest, and one during an intravenous alcohol infusion, with a prescribed ascent to a target breath alcohol concentration (BrAC), at which it was then "clamped." The alcohol clamp was started 5min after scan start, with a linear increase in BrAC over 15min to the target of 80mg%, the legal threshold for intoxication. Target BrAC was maintained for 30min. Voxel-wise binding potential (BPND) was estimated with MRTM2. RESULTS: IV EtOH induced significant increases in DA in the right ventral striatum in NTS, but not SD. No decreases in DA were observed in either group. CONCLUSIONS: Alcohol intoxication results in distinct anatomic profiles of DA responses in SD and NTS, suggesting that in NTS, the striatal DA system may process effects of alcohol intoxication differently than in SD.
BACKGROUND: Striatal dopamine (DA) has been implicated in alcohol use disorders, but it is still unclear whether or not alcohol can induce dopamine release in social drinkers. Furthermore, no data exist on dopamine responses to alcohol in dependent drinkers. We sought to characterize the DA responses to alcohol intoxication in moderately large samples of social drinkers (SD) and nontreatment-seeking alcoholics (NTS). METHODS: Twenty-four SD and twenty-one NTS received two [(11)C]raclopride (RAC) PET scans; one at rest, and one during an intravenous alcohol infusion, with a prescribed ascent to a target breath alcohol concentration (BrAC), at which it was then "clamped." The alcohol clamp was started 5min after scan start, with a linear increase in BrAC over 15min to the target of 80mg%, the legal threshold for intoxication. Target BrAC was maintained for 30min. Voxel-wise binding potential (BPND) was estimated with MRTM2. RESULTS: IV EtOH induced significant increases in DA in the right ventral striatum in NTS, but not SD. No decreases in DA were observed in either group. CONCLUSIONS:Alcohol intoxication results in distinct anatomic profiles of DA responses in SD and NTS, suggesting that in NTS, the striatal DA system may process effects of alcohol intoxication differently than in SD.
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