Abstract
While the deleterious effects of acute ethyl alcohol intoxication on executive control are well-established, the underlying spatiotemporal brain mechanisms remain largely unresolved. In addition, since the effects of alcohol are noticeable to participants, isolating the effects of the substance from those related to expectations represents a major challenge. We addressed these issues using a double-blind, randomized, parallel, placebo-controlled experimental design comparing the behavioral and electrical neuroimaging acute effects of 0.6 vs 0.02 g/kg alcohol intake recorded in 65 healthy adults during an inhibitory control Go/NoGo task. Topographic ERP analyses of covariance with self-reported dose expectations allowed to dissociate their neurophysiological effects from those of the substance.While alcohol intoxication increased response time variability and post-error slowing, bayesian analyses indicated that it did not modify commission error rates. Functionally, alcohol induced topographic ERP modulations over the periods of the stimulus-locked N2 and P3 components, arising from pre-supplementary motor and anterior cingulate areas. In contrast, alcohol decreased the strength of the response-locked anterior cingulate error-related component but not its topography. This pattern indicates that alcohol had a locally specific influence within the executive control network, but disrupted performance monitoring processes via global strength-based mechanisms.We further revealed that alcohol-related expectations induced temporally specific functional modulations of the early N2 stimulus-locked medio-lateral prefrontal activity, a processing phase preceding those influenced by the actual alcohol intake.Our collective findings thus not only reveal the mechanisms underlying alcohol-induced impairments in impulse control and error processing, but also dissociate substance- from expectations- related functional effects.
Highlights
The association between acute ethyl alcohol intoxication and impulsive behaviors has been advanced to follow from its deleterious effect on executive functions (George et al, 2005; Giancola, 2000; MacDonald et al, 1996)
We further revealed that alcohol-related expectations induced temporally specific functional modulations of the early N2 stimulus-locked medio-lateral prefrontal activity, a processing phase preceding those influenced by the actual alcohol intake
Since most our behavioral dependent variables were not normally distributed, we report medians and interquartile ranges (IQR; Table 3; following the recommandations by Habibzadeh, 2013), and submitted all our behavioral dependent variables to non-parametric Mann-Whitney test (Monte Carlo bootstrapping with 100000 samples using SPSS Statistics 25 software, IBM Corp, Armonk, NY)
Summary
The association between acute ethyl alcohol intoxication and impulsive behaviors has been advanced to follow from its deleterious effect on executive functions (George et al, 2005; Giancola, 2000; MacDonald et al, 1996). Less than ten studies examined the functional correlates of acute alcohol intoxication during executive control tasks in healthy occasional drinkers These studies are scant, and involved methods with either limited temporal (fMRI, NIRS) or spatial resolution (event-related potentials) and focused on either stimulus-locked or response-locked activity. These limitations left unresolved whether alcohol impairs feed-forward processes such as attentional capture and stimulus-response mapping and/or later latency conflict detection or topdown motoric inhibition, and hamper the establishment of a global, integrative view of the neurophysiological effects of acute intoxication. Event-related potentials studies consistently revealed that acute intoxication reduces inhibition P3 components (Bartholow et al, 2003; Easdon et al, 2005), error processing ERN and Pe components (Bailey et al, 2014; Easdon et al, 2005; Ridderinkhof et al, 2002), as well as evaluative and regulative N450 and NSW components (Curtin and Fairchild, 2003)
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