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Often seen as the paragon of higher cognition, here we suggest that cognitive control is dependent on emotion. Rather than asking whether control is influenced by emotion, we ask whether control itself can be understood as an emotional process. Reviewing converging evidence from cybernetics, animal research, cognitive neuroscience, and social and personality psychology, we suggest that cognitive control is initiated when goal conflicts evoke phasic changes to emotional primitives that both focus attention on the presence of goal conflicts and energize conflict resolution to support goal-directed behavior. Critically, we propose that emotion is not an inert byproduct of conflict but is instrumental in recruiting control. Appreciating the emotional foundations of control leads to testable predictions that can spur future research.

Errors in timed choice tasks typically produce an error-related negativity (ERN) in the event-related potential (ERP). The error specificity of the ERN has been challenged by studies showing a correct response negativity (CRN). Forty-five participants engaged in a flanker task in which both compatibility between flankers and target and the probability of compatible flankers were manipulated. Correct responses elicited a CRN, the amplitude of which increased with the degree of mismatch between the presence of conflict and conflict probability, even on low-conflict (compatible) trials. The fronto-central N2 component was larger on high-conflict (incompatible) correct response trials. However, in contrast to some recent accounts, this N2 was largest for highly probable stimuli. These findings suggest revision to models of the effects of conflict on response-related negativity to account for strategic adjustments made in preparation for the response.

The personality systems of Cloninger (as measured by the Tridimensional Personality Questionnaire [TPQ]) and Eysenck (as measured by the Eysenck Personality Questionnaire [EPQ]) both have been linked to substance use and abuse. The current study examined the predictive utility of both systems for substance use disorder (SUD) diagnoses, both cross-sectionally and prospectively. Participants (N = 489 at baseline) completed the EPQ and TPQ and were assessed via structured diagnostic interview at baseline and 6 years later (N = 457 at follow-up). Both the EPQ and TPQ scales demonstrated bivariate cross-sectional and prospective associations with SUDs. Within each system, those dimensions marking a broad impulsive sensation-seeking or behavioral disinhibition trait were the best predictors prospectively, although the 2 systems were differentially sensitive to specific diagnoses. These relations remained significant even with autoregressivity, other concurrent SUD diagnoses, and multiple personality dimensions statistically controlled.

No abstract

Behavioral analyses are a natural choice for understanding the wide-ranging behavioral consequences of racial stereotyping and prejudice. However, neuroimaging and electrophysiological research has recently considered the neural mechanisms that underlie racial categorization and the activation and application of racial stereotypes and prejudice, revealing exciting new insights. Work reviewed here points to the importance of neural structures previously associated with face processing, semantic knowledge activation, evaluation, and self-regulatory behavioral control, allowing for the specification of a neural model of race processing. We show how research on the neural correlates of race can serve to link otherwise disparate lines of evidence on the neural underpinnings of a broad array of social-cognitive phenomena, and consider implications for effecting change in race relations.

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. Alcohol reduced both the ERN and error positivity (Pe) components of the ERP following errors and impaired typical posterror behavioral adjustment. Structural equation modeling indicated that effects of alcohol on both the ERN and posterror adjustment were significantly mediated by reductions in NA. Effects of alcohol on Pe amplitude were unrelated to posterror adjustment, however. These findings indicate a role for affect modulation in understanding alcohol’s effects on self-regulatory impairment and more generally support theories linking the ERN with a distress-related response to control failures.

Two experiments tested the hypothesis that alcohol increases race-biased responding via impairment of self-regulatory cognitive control. Participants consumed either a placebo or alcohol and then made speeded responses to stereotypic trait words presented after White and Black face primes while behavioral and event-related brain potential (ERP) data were recorded. Alcohol did not affect stereotype activation in either experiment. Experiment 2 showed that alcohol significantly impaired the ability to inhibit race-biased responses but did not reliably influence control of counterstereotypic responses. This disinhibition appears driven by impairment of regulative cognitive control, as indexed by amplitude of the negative slow wave ERP component. These findings suggest that controlling racial bias can be a function of effective implementation of basic self-regulatory processes in addition to the motivational processes identified in other research.