4.7 Article

Neural correlates of inhibitory control are associated with stimulant-like effects of alcohol

Journal

NEUROPSYCHOPHARMACOLOGY
Volume 46, Issue 8, Pages 1442-1450

Publisher

SPRINGERNATURE
DOI: 10.1038/s41386-021-01014-5

Keywords

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Funding

  1. National Institute on Drug Abuse Grants [R01 DA002812, R21 DA037642]
  2. National Institute on Alcohol Abuse and Alcoholism grant [K01 AA024519, K01 AA025111, P60 AA007611]

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Poor inhibitory control and heightened feelings of stimulation are two well-established risk factors for AUD, and recent evidence suggests they are related and may share common neurobiological mechanisms. Subjective reports of stimulation following alcohol were inversely associated with brain activity during inhibition, while feelings of sedation did not correlate with brain activation.
Poor inhibitory control and heightened feelings of stimulation after alcohol are two well-established risk factors for alcohol use disorder (AUD). Although these risk factors have traditionally been viewed as orthogonal, recent evidence suggests that the two are related and may share common neurobiological mechanisms. Here we examined the degree to which neural activity during inhibition was associated with subjective reports of stimulation following alcohol. To assess neural changes during inhibition, moderate alcohol drinkers performed a stop signal task during fMRI without drug. To assess subjective responses to alcohol they ingested alcohol (0.8 g/kg) or placebo beverages under double-blind conditions and provided subjective reports of stimulation and sedation. Feelings of stimulation following alcohol were inversely associated with activity in the supplementary motor area, insula, and middle frontal gyrus during inhibition (successful stop trials compared to go trials). Feelings of sedation did not correlate with brain activation. These results extend previous findings suggesting that poor inhibitory control is associated with more positive subjective responses to alcohol. These interrelated risk factors may contribute to susceptibility to future excessive alcohol use, and ultimately lead to neurobiological targets to prevent or treat AUD.

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