system supporting the rapid evaluation of unfavorable outcomes was not modulated by alcohol. In line with our hypothesis, feedback-related P300 amplitudes in response to negative feedback (i.e., balloon bursts) were reduced in alcohol-intoxicated individuals as compared to sober controls, and this group difference was absent in response to positive feedback. Hence, our behavioral observations corroborate the ERP results, demonstrating that early feedback processing, as indexed by the FRN, remained intact after alcohol consumption, enabling participants to modify behavior from trial to trial in accordance to feedback. Alcohol-intoxicated participants, in contrast to the participants in the placebo condition, nevertheless failed to achieve the most optimal strategy on the long run. This could be explained by the diminished P300 amplitudes to losses. The P300 is traditionally associated with context updating in working memory. Here, blunted P300 amplitudes may reflect less effective integration of past occurrences of outcomes, particularly penalties, over the course of the task. Consequently, our ERP findings suggest that it is not the ability to rapidly evaluate feedback valence that is influenced by alcohol consumption, but rather the ability to subsequently assign sufficient attention to further process motivationally salient events. Hence, alcohol prevented these participants from building a reinforcement history
