Microdialysis experiments in rodents indicate that ethanol promotes dopamine release predominantly in the nucleus accumbens, a phenomenon that is implicated in the reinforcing effects of drugs of abuse. The aim of the present study was to test the hypothesis in humans that an oral dose of ethanol would lead to dopamine release in the ventral striatum, including the nucleus accumbens. Six healthy subjects underwent two [(11)C]raclopride PET scans following either alcohol (1 ml/kg) in orange juice or orange juice alone. Subjective mood changes, heart rate, and blood-alcohol levels were monitored throughout the procedure. Personality traits were evaluated using the tridimensional personality questionnaire. PET images were co-registered with MRI and transformed into stereotaxic space. Statistical parametric maps of [(11)C]raclopride binding potential change were generated. There was a significant reduction in [(11)C]raclopride binding potential bilaterally in the ventral striatum/nucleus accumbens in the alcohol condition compared to the orange juice condition, indicative of increased extracellular dopamine. Moreover, the magnitude of the change in [(11)C]raclopride binding correlated with the alcohol-induced increase in heart rate, which is thought to be a marker of the psychostimulant effects of the drug, and with the personality dimension of impulsiveness. The present study is the first report that, in humans, alcohol promotes dopamine release in the brain, with a preferential effect in the ventral striatum. These findings support the hypothesis that mesolimbic dopamine activation is a common property of abused substances, possibly mediating their reinforcing effects.

Histories of violence and of hyperactivity are both characterized by poor cognitive-neuropsychological function. However, researchers do not know whether these histories combine in additive or interactive ways. The authors tested 303 male young adults from a community sample whose trajectories of teacher-rated physical aggression and motoric hyperactivity from kindergarten to age 15 were well defined. No significant interaction was found. In a 1st model, both histories of problem behavior were independently associated with cognitive-neuropsychological function in most domains. In a second model controlling for IQ, General Memory, and test motivation, none of the three Working Memory tests (relevant to executive function) remained associated with physical aggression or hyperactivity. These results support an additive model but no specificity to executive function [corrected].

Novelty/sensation-seeking is among the personality traits that have been linked to heavy alcohol use. This study suggests that reward sensitivity might mediate the relationship between this personality profile and drinking behavior.