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. 2016 Mar 1:160:163-9.
doi: 10.1016/j.drugalcdep.2016.01.001. Epub 2016 Jan 13.

Differences in IV alcohol-induced dopamine release in the ventral striatum of social drinkers and nontreatment-seeking alcoholics

Karmen K Yoder  1 , Daniel S Albrecht  2 , Mario Dzemidzic  3 , Marc D Normandin  4 , Lauren M Federici  5 , Tammy Graves  6 , Christine M Herring  5 , Karen L Hile  5 , James W Walters  5 , Tiebing Liang  7 , Martin H Plawecki  8 , Sean O'Connor  9 , David A Kareken  10
Affiliations

Differences in IV alcohol-induced dopamine release in the ventral striatum of social drinkers and nontreatment-seeking alcoholics

Karmen K Yoder et al. Drug Alcohol Depend. .

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.

Keywords: Alcohol; Dopamine; Positron emission tomography; Raclopride; Ventral striatum.

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Figures

Figure 1
Figure 1
Typical study day timeline. RAC = [11C]raclopride PET scan; ICRC = Indiana Clinical Research Center.
Figure 2
Figure 2
Subjective ratings for “high” during the alcohol RAC PET scan. Left y-axis, visual analog ratings for “high” for SD (filled circles, black line) and NTS (open circles, dotted line). Data are mean ± s.d. Data were not available for one NTS subject. Alcohol infusion was started 5 minutes after the RAC injection (t = 0; gray arrow). The BrAC target for the 30 minute IV alcohol clamp (gray bar) was 80 mg%. See text for details.
Figure 3
Figure 3
Voxel-wise results for main effect of alcohol across all subjects, indicating where IV ethanol increased dopamine relative to the resting baseline [BPND-rest > BPND-alcohol]. See text for details. Display height, p < 0.005, uncorrected; cluster extent threshold k = 20 voxels. Color bar indicates the t-statistic. See text for details. The magnitudes of ΔBPND from each cluster, by group, are presented in Table 4.
See this image and copyright information in PMC

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