Dataset Information

Effects of acute alcohol intoxication on saccadic conflict and error processing.

ABSTRACT: 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.

SUBMITTER: Marinkovic K

PROVIDER: S-EPMC3869380 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Effects of acute alcohol intoxication on saccadic conflict and error processing.

Marinkovic Ksenija K Rickenbacher Elizabeth E Azma Sheeva S Artsy Elinor E Lee Adrian K C AK

Psychopharmacology 20130628 3

<h4>Rationale</h4>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 ...[more]

PMID: 23812762

Similar Datasets

Project description:Alcohol intoxication can increase inflammation and worsen injury, yet the mechanisms involved are not clear. We investigated whether acute alcohol intoxication increases microvascular permeability and investigated potential signaling mechanisms in endothelial cells that may be involved.Conscious rats received a 2.5 g/kg alcohol bolus via gastric catheters to produce acute intoxication. Microvascular leakage of intravenously administered fluorescein isothiocyanate (FITC)-conjugated albumin (FITC-albumin) from the mesenteric microcirculation was assessed by intravital microscopy. Endothelial-specific mechanisms were studied using cultured endothelial cell monolayers. Transendothelial electrical resistance (TER) served as an index of barrier function, before and after treatment with alcohol or its metabolite acetaldehyde. Pharmacologic agents were used to test the roles of alcohol metabolism, oxidative stress, p38 mitogen-activated protein kinase (MAPK), myosin light-chain kinase (MLCK), rho kinase (ROCK), and exchange protein activated by cAMP (Epac). VE-cadherin localization was investigated to assess junctional integrity. Rac1 and RhoA activation was assessed by ELISA assays.Alcohol significantly increased FITC-albumin extravasation from the mesenteric microcirculation. Alcohol also significantly decreased TER and disrupted VE-cadherin organization at junctions. Acetaldehyde significantly decreased TER, but inhibition of alcohol dehydrogenase or application of a superoxide dismutase mimetic failed to prevent alcohol-induced decreases in TER. Inhibition of p38 MAPK, but not MLCK or ROCK, significantly attenuated the alcohol-induced barrier dysfunction. Alcohol rapidly decreased GTP-bound Rac1 but not RhoA during the drop in TER. Activation of Epac increased TER, but did not prevent alcohol from decreasing TER. However, activation of Epac after initiation of alcohol-induced barrier dysfunction quickly resolved TER to baseline levels.Our results suggest that alcohol intoxication increases microvascular permeability to plasma proteins. The data also suggest the endothelial-specific mechanism involves the p38 MAPK, Rac1, and reorganization of VE-cadherin at junctions. Last, activation of Epac can quickly resolve alcohol-induced endothelial barrier dysfunction.

Project description:The detrimental effects of acute alcohol intoxication and long-term alcohol (ab)use on cognition are well-known. Yet, only little is known about the cognitive effects of an acute alcohol hangover, even though it might affect executive functions associated with workplace performance or driving skills. Given that alcohol hangover may increase the speed of information accumulation, we assessed the behavioral effects of conflict load (induced by a subliminal prime) on cognitive control, as assessed via the Flanker effect. We employed a counter-balanced within-subject design, where n = 25 healthy young males were tested once after a sober night and once after a night of experimentally induced heavy drinking of cheap brandy/red wine (2.6375 g alcohol per estimated liter of body water within 2-3 h). Alcohol hangover neither increased the cognitive conflicts induced by consciously processed distractors alone (i.e., the Flanker effect), nor modulated conflict adaptation (i.e., the Gratton effect). Instead, hangover potentiated the detrimental effects of conflicting subliminal primes on top-down cognitive conflicts. This effect was likely due to an increase in the speed of information accumulation from visual stimuli and the resulting increase in subliminal conflict load induced by incompatible primes. We further found the size of this effect to be positively correlated with age and subjective sleepiness during the hangover state, but the hangover effect remained significant even after correcting for those covariates. We further found no correlation of the behavioral effect with the subjective overall rating of hangover symptoms or the maximal breath alcohol concentration reached during prior intoxication. Taken together, our findings suggest that alcohol hangover may affect cognitive performance due to an increase in non-conscious processing of visual distractors. While the size of this effect might increase with age and sleepiness, it is not entirely dependent on those covariates and not necessarily related to subjective ratings of general hangover symptoms/impairment.

Dataset Information

Effects of acute alcohol intoxication on saccadic conflict and error processing.

Publications

Effects of acute alcohol intoxication on saccadic conflict and error processing.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets