Citation

Nikolaou K, Field M, Critchley H, Duka T. Neuropsychopharmacology 2013; 38(7): 1365-1373.

Affiliation

Behavioural and Clinical Neuroscience, School of Psychology, University of Sussex, Brighton, UK.

Copyright

(Copyright © 2013, Nature Publishing Group)

DOI

10.1038/npp.2013.34

PMID

23361162

Abstract

Acute alcohol ingestion increases attentional bias to alcohol-related stimuli; however the underlying cognitive and brain mechanisms remain unknown. We combined functional magnetic resonance imaging (fMRI) with performance of a dual task that probed attentional distraction by alcohol-related stimuli during 'conflict' processing; the Concurrent Flanker/Alcohol-Attentional bias task (CFAAT). In this task, an Eriksen Flanker task is superimposed on task-unrelated background pictures with alcohol-associated or neutral content. Participants respond to the direction of a central 'target' arrow and ignore adjacent congruent (low cognitive load) or incongruent (high cognitive load) 'flanking' arrows. Using a between-subject design, forty healthy moderate-to-heavy social drinkers received either no alcohol (placebo), 0.4 g/kg (low dose) or 0.8 g/kg (high dose) of alcohol, and underwent fMRI while performing the CFAAT. The low alcohol-dose, relative to placebo, increased response latencies on trials with alcohol-associated backgrounds and, under low cognitive load, increased the activity evoked by these pictures within a medial hypothalamic region. Under high cognitive load, the low alcohol-dose, relative to placebo, elicited greater activity within a more lateral hypothalamic region, and reduced activity within frontal motor areas. The high alcohol-dose, relative to placebo, did not reliably affect response latencies or neural responses to background images, but reduced overall accuracy under high cognitive load. This effect correlated with changes in reactivity within medial and dorsal prefrontal cortices. These data suggest that alcohol at a low dose primes attentional bias to alcohol-associated stimuli, an effect mediated by activation of subcortical hypothalamic areas implicated in arousal and salience attribution.Neuropsychopharmacology accepted article preview online, 29 January 2013;. doi:10.1038/npp.2013.34.

Language: en