Psychological Sciences

Alcohol is known to impair self-regulatory control of behavior, though mechanisms for this effect remain unclear. Here, we tested the hypothesis that alcohol"s reduction of negative affect (NA) is a key mechanism for such impairment. This hypothesis was tested by measuring the amplitude of the error-related negativity (ERN), a component of the event-related brain potential (ERP) posited to reflect the extent to which behavioral control failures are experienced as distressing, while participants completed a laboratory task requiring self-regulatory control.

Numerous externalizing behaviors, from aggression to risk taking to drug abuse, stem from impaired cognitive control, including that brought about by the acute effects of alcohol. Although research generally indicates that alcohol impairs cognitive abilities, a close examination of the literature suggests that alcohol's effects are quite variable and likely depend on a number of contextual factors. The purpose of the current study was to characterize the effects of alcohol on cognitive control in terms of neural and behavioral responses to successful and unsuccessful control attempts. Participants were randomly assigned to consume an alcohol (0.80g/kg ETOH), placebo, or nonalcoholic control beverage prior to completing a cognitive control (flanker) task while event-related brain potentials were recorded. Alcohol reduced the amplitude of the error-related negativity on error trials and increased the posterror compatibility effect in response time. Of particular interest, neural indices of conflict monitoring and performance adjustment (frontal slow wave) were attenuated by alcohol, but only on trials following errors. These functions had recovered, however, by 2 trials after an error. These findings suggest that alcohol's effects on cognitive control are best characterized as impaired (or delayed) recovery following control failures. Implications of these findings for understanding alcohol's effects on behavioral undercontrol are discussed.

This experiment investigated the role of conflict in the response and evaluative categorization systems in the affective congruency effect using event-related brain potentials (ERPs). Participants completed a primed evaluative decision task in which the proportion of congruent to incongruent trials was manipulated. The size of the affective congruency effect increased along with the proportion of congruent trials. ERP data identified the locus of this effect in the response system: the lateralized readiness potential (LRP) showed that preferential response activation occurred in motor cortex following prime onset, and the fronto-central N2 (conflict monitoring) component indicated that conflict occurred when the response activated by the prime differed from the target response, irrespective of the affective congruency of the prime and target. The extent of this conflict covaried with strategic processing of primes, as participants directed less attention to primes that were likely to elicit conflict. These data support a response conflict account of affective congruency effects in the evaluative decision task and indicate that strategic control of attention is important in determining the extent to which conflict occurs.

Previous research has shown that alcohol consumption can increase the expression of race bias by impairing control-related processes. The current study tested whether simple exposure to alcohol-related images can also increase bias, but via a different mechanism. Participants viewed magazine ads for either alcoholic or nonalcoholic beverages prior to completing Payne's (2001) Weapons Identification Task (WIT). As predicted, participants primed with alcohol ads exhibited greater race bias in the WIT than participants primed with neutral beverages. Process dissociation analyses indicated that these effects were due to automatic (relative to controlled) processes having a larger influence on behavior among alcohol-primed relative to neutralprimed participants. Structural equation modeling further showed that the alcohol-priming effect was mediated by increases in the influence of automatic associations on behavior. These data suggest an additional pathway by which alcohol can potentially harm inter-racial interactions, even when no beverage is consumed.