Moderate acute alcohol use impairs intentional inhibition rather than stimulus-driven inhibition

Abstract

Moderate alcohol intake may impair stimulus-driven inhibition of motor actions in go/no-go and stop-signal tasks. Exposure to alcohol-related cues has been found to exacerbate this impairment. By contrast, the effect of alcohol use on intentional inhibition, or the capacity to voluntarily suspend an action, has rarely been investigated. We examined whether and how moderate alcohol intake affects stimulus-driven inhibition (stop-signal task) and intentional inhibition (chasing bottles task), during exposure to alcohol-related stimuli. One hundred and eleven participants were randomly assigned to an alcohol (male: 0.55 g/kg, female: 0.45 g/kg), placebo, or control group. For the stop-signal task, ANOVAs were performed on stop-signal reaction time (SSRT) and go RT with Pharmacological and Expectancy Effects of Alcohol, Stimulus Category (alcohol-related or neutral), and Sex as factors. For the chasing bottles task, multilevel survival analysis was performed to predict whether and when intentional inhibition was initiated, with the same factors. For the stop-signal task, Sex moderated the Pharmacological Effect of Alcohol on SSRT: only for females, alcohol consumption shortened SSRT. In the non-alcohol groups, males had shorter SSRT than females. Concerning intentional inhibition, the alcohol group initiated intentional inhibition less often, especially when stimuli were non-alcohol related. These findings indicate that (1) stimulus-driven inhibition and intentional inhibition reflect different aspects of response inhibition; (2) moderate alcohol intake negatively affects intentional inhibition (but not stimulus-driven inhibition). Speculatively, the observed impairment in intentional inhibition might underlie the lack of control over alcohol drinking behavior after a priming dose. This study highlights the potential role of intentional inhibition in the development of addiction.

Aldehyde dehydrogenase 2–associated changes in pharmacokinetics, locomotor function and peripheral glutamic acid and gamma-aminobutyric acid levels during acute alcohol intoxication in male mice

“…The mutation results in a substitution of lysine for glutamate at position 487 of the human ALDH2 protein and the corresponding decrease in enzymatic activity. When challenged with moderate and high doses of alcohol (0.4–0.8 g/kg) (Liu et al , 2021), human ALDH2*2 heterozygotes show enhanced increases in acetaldehyde levels in the blood and exhibit significantly impaired psychomotor performance (Shin et al , 2006; Kim et al , 2010).…”

Anti-saccade as a Tool to Evaluate Neurocognitive Impairment in Alcohol Use Disorder

“…The cognitive processes include in such tasks involve both manual inhibition and saccade inhibition. Alcohol can also affect the motoric execution, such as the button press ( 82 ).…”