Effects of acute alcohol intoxication on saccadic conflict and error processing
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Flexible behavior optimization relies on cognitive control which includes the ability to suppress automatic responses interfering with relevant goals. Extensive evidence suggests that the anterior cingulate cortex (ACC) is the central node in a predominantly frontal cortical network subserving executive tasks. Neuroimaging studies indicate that the ACC is sensitive to acute intoxication during conflict, but such evidence is limited to tasks using manual responses with arbitrary response contingencies.
The present study was designed to examine whether alcohol's effects on top–down cognitive control would generalize to the oculomotor system during inhibition of hardwired saccadic responses.
Healthy social drinkers (N = 22) underwent functional magnetic resonance imaging (fMRI) scanning and eye movement tracking during alcohol (0.6 g/kg ethanol for men, 0.55 g/kg for women) and placebo conditions in a counterbalanced design. They performed visually guided prosaccades (PS) towards a target and volitional antisaccades (AS) away from it. To mitigate possible vasoactive effects of alcohol on the BOLD (blood oxygenation level-dependent) signal, resting perfusion was quantified with arterial spin labeling (ASL) and used as a covariate in the BOLD analysis.
Saccadic conflict was subserved by a distributed frontoparietal network. However, alcohol intoxication selectively attenuated activity only in the ACC to volitional AS and erroneous responses.
This study provides converging evidence for the selective ACC vulnerability to alcohol intoxication during conflict across different response modalities and executive tasks, confirming its supramodal, high-level role in cognitive control. Alcohol intoxication may impair top–down regulative functions by attenuating the ACC activity, resulting in behavioral disinhibition and decreased self-control.
KeywordsAnterior cingulate cortex Cognitive control Antisaccades Alcohol intoxication Error-related activity Arterial spin labeling (ASL)
This work was supported by funds from the National Institutes of Health (R01-AA016624 and P41RR14075) and Medical Investigation of Neurodevelopmental Disorders (MIND) Institute. Data were collected at the MGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging. Authors report no financial or other conflict of interest related to this work. We thank Simon Sigalovsky, Matija Zelic, Sarah Sheldon, Roya Bagheri, Lawrence Wald, and Dara Manoach for assistance.
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