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"Free won't" after a beer or two: chronic and acute effects of alcohol on neural and behavioral indices of intentional inhibition.

ABSTRACT: BACKGROUND:Response inhibition can be classified into stimulus-driven inhibition and intentional inhibition based on the degree of endogenous volition involved. In the past decades, abundant research efforts to study the effects of alcohol on inhibition have focused exclusively on stimulus-driven inhibition. The novel Chasing Memo task measures stimulus-driven and intentional inhibition within the same paradigm. Combined with the stop-signal task, we investigated how alcohol use affects behavioral and psychophysiological correlates of intentional inhibition, as well as stimulus-driven inhibition. METHODS:Experiment I focused on intentional inhibition and stimulus-driven inhibition in relation to past-year alcohol use. The Chasing Memo task, the stop-signal task, and questionnaires related to substance use and impulsivity were administered to 60 undergraduate students (18-25 years old). Experiment II focused on behavioral and neural correlates acute alcohol use on performance on the Chasing Memo task by means of electroencephalography (EEG). Sixteen young male adults (21-28 years old) performed the Chasing Memo task once under placebo and once under the influence of alcohol (blood alcohol concentration around 0.05%), while EEG was recorded. RESULTS:In experiment I, AUDIT (Alcohol Use Disorder Identification Test) total score did not significantly predict stimulus-driven inhibition or intentional inhibition performance. In experiment II, the placebo condition and the alcohol condition were comparable in terms of behavioral indices of stimulus-driven inhibition and intentional inhibition as well as task-related EEG patterns. Interestingly, a slow negative readiness potential (RP) was observed with an onset of about 1.2 s, exclusively before participants stopped intentionally. CONCLUSIONS:These findings suggest that both past-year increases in risky alcohol consumption and moderate acute alcohol use have limited effects on stimulus-driven inhibition and intentional inhibition. These conclusions cannot be generalized to alcohol use disorder and high intoxication levels. The RP might reflect processes involved in the formation of an intention in general.

SUBMITTER: Liu Y

PROVIDER: S-EPMC6947965 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:RATIONALE:Compared to the general population, adult Attention-Deficit / Hyperactivity Disorder (ADHD) is more prevalent in patients with Alcohol Use Disorder (AUD). Impaired behavioral inhibition is a common characteristic in both ADHD and AUD. Relapse risk is increased in patients with AUD and comorbid, untreated ADHD and in AUD patients with increased neural cue-reactivity. OBJECTIVES:In this study, we examined the interaction between neural correlates of behavioral inhibition and alcohol cue-reactivity with a hybrid imaging task. METHODS:Out of 69 adult study participants, we included n?=?49 in our final analyses: Individuals had a diagnosis of either AUD (n?=?13), ADHD (n?=?14) or both (n?=?5), or were healthy controls (HC; n?=?17). The functional magnetic resonance imaging paradigm aimed to examine the combined effects of both an interference-inhibition task ("Simon-task") and an alcohol cue-reactivity task. Instead of segregating by diagnostic group, we pursued a dimensional approach in which we compared measures of AUD and ADHD severity, as well as the interaction of both, using multiple regression analyses. RESULTS:The four groups did not differ on the behavioral level on either the inhibition task or the alcohol cue-reactivity task. However, brain activation in frontal control and reward-related regions during completion of the combined tasks were related to ADHD and AUD severity (symptom load). During presentation of both alcohol cues and the inhibition task, participants with higher AUD and ADHD symptom load exhibited greater BOLD (blood oxygen level dependent) responses in subcortical reward-related regions. CONCLUSIONS:Our findings support the hypothesis that ADHD additionally diminishes inhibition ability in individuals with AUD. This may increase relapse risk when confronted with alcohol cues. Further, it is crucial for patients with comorbid AUD and ADHD to take into account not only reduced cognitive control over behavioral inhibition but also simultaneously heightened alcohol cue-reactivity.

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"Free won't" after a beer or two: chronic and acute effects of alcohol on neural and behavioral indices of intentional inhibition.

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