Binge drinking and the differential influence of ethanol on cognitive control subprocesses: a novel field of neurotoxicology

Stock, Ann‐Kathrin; Beste, Christian

doi:10.1007/s00204-013-1172-8

Cited by 9 publications

(8 citation statements)

References 13 publications

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“…We used the "Alcotest 3000" breathalyzer (Drägerwerk, Lübeck, Germany) to assess BrAC at the beginning of each appointment (sober task performance, intoxicated task performance, MRS acquisition) and immediately before/after each task during the intoxicated appointment. Importantly, previous publications [47,57] have demonstrated that the obtained breath alcohol levels essentially yield the same results as a capillary gas chromatography-headspace analysis of venous blood. For the MRS acquisition, participants were invited to a third and separate sober scanning appointment, which also had to be within one week of testing, and no less than 48 h after the drinking appointment.…”

Section: Experimental Design and Alcohol Administrationmentioning

confidence: 59%

Acute Alcohol Effects on Response Inhibition Depend on Response Automatization, but not on GABA or Glutamate Levels in the ACC and Striatum

Bensmann

Zink

Werner

et al. 2020

JCM

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Alcohol increases GABAergic signaling and decreases glutamatergic signaling in the brain. Variations in these neurotransmitter levels may modulate/predict executive functioning. Matching this, strong impairments of response inhibition are one of the most consistently reported cognitive/behavioral effects of acute alcohol intoxication. However, it has never been investigated whether baseline differences in these neurotransmitters allow to predict how much alcohol intoxication impairs response inhibition, and whether this is reflected in neurophysiological measures of cognitive control. We used MR spectroscopy to assess baseline (i.e., sober) GABA and glutamate levels in the anterior cingulate cortex (ACC) and striatum in n = 30 healthy young males, who were subsequently tested once sober and once intoxicated (1.01 permille). Inhibition was assessed with the sustained attention to response task (SART). This paradigm also allows to examine the effect of different degrees of response automatization, which is a known modulator for response inhibition, but does not seem to be substantially impaired during acute intoxication. As a neurophysiological correlate of response inhibition and control, we quantified EEG-derived theta band power and located its source using beamforming analyses. We found that alcohol-induced response inhibition deficits only occurred in the case of response automatization. This was reflected by decreased theta band activity in the left supplementary motor area (SMA), which may reflect modulations in the encoding of a surprise signal in response to inhibition cues. However, we did not find that differences in baseline (i.e., sober) GABA or glutamate levels significantly modulated differences in the size of alcohol-induced inhibition deficits.

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Section: Experimental Design and Alcohol Administrationmentioning

confidence: 59%

Acute Alcohol Effects on Response Inhibition Depend on Response Automatization, but not on GABA or Glutamate Levels in the ACC and Striatum

Bensmann

Zink

Werner

et al. 2020

JCM

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“…This indicates that high‐dose ethanol intoxication seems to reduce the degree of conflict in situations where switching processes are ‘self‐initiated’ and need to be recalled out of memory. With regard to the behavioral results, it can therefore be assumed that strongly demanding situations, like memory‐based switching processes, need a certain amount of cognitive control (Stock and Beste ; Stock et al ; Stock et al ) in order to result in diminished switch costs and thus in increased performance. The sLORETA analysis reveals that this difference results from activation differences in the anterior cingulate cortex (ACC), which replicates findings showing that processes of response selection and control seem to be medicated by the ACC (Botvinick ; Folstein and Van Petten ; Gajewski et al ).…”

Section: Discussionmentioning

confidence: 99%

“…While it is well‐known that different cognitive functions may already become impaired at lower ethanol intoxication levels (i.e. between 0.3 and 0.8‰), it has been shown that even at high intoxication levels (≥1.2‰), effects on cognitive functions remain rather specific: While response selection and control processes are predominantly affected, attentional selection processes are largely left unaffected (Stock and Beste ; Stock et al ; Stock et al ). Those studies suggest that binge drinking mainly compromises cognitive functions that strongly depend on prefrontal cortical and striatal processes.…”

Section: Introductionmentioning

confidence: 99%

“…cue‐based and memory‐based task switching might be equally affected. However, some findings suggest that even high‐dose ethanol intoxication only affects cognitive control processes when there are likely to be strongly demanded (Stock and Beste ; Stock et al ; Stock et al ). It is therefore also possible that switching is more strongly affected in the memory‐based task version than in the less demanding cue‐based task version.…”

Section: Introductionmentioning

confidence: 99%

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Effects of high‐dose ethanol intoxication and hangover on cognitive flexibility

et al. 2016

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The effects of high-dose ethanol intoxication on cognitive flexibility processes are not well understood, and processes related to hangover after intoxication have remained even more elusive. Similarly, it is unknown in how far the complexity of cognitive flexibility processes is affected by intoxication and hangover effects. We performed a neurophysiological study applying high density electroencephalography (EEG) recording to analyze event-related potentials (ERPs) and perform source localization in a task switching paradigm which varied the complexity of task switching by means of memory demands. The results show that high-dose ethanol intoxication only affects task switching (i.e. cognitive flexibility processes) when memory processes are required to control task switching mechanisms, suggesting that even high doses of ethanol compromise cognitive processes when they are highly demanding. The EEG and source localization data show that these effects unfold by modulating response selection processes in the anterior cingulate cortex. Perceptual and attentional selection processes as well as working memory processes were only unspecifically modulated. In all subprocesses examined, there were no differences between the sober and hangover states, thus suggesting a fast recovery of cognitive flexibility after high-dose ethanol intoxication. We assume that the gamma-aminobutyric acid (GABAergic) system accounts for the observed effects, while they can hardly be explained by the dopaminergic system.

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“…These studies revealed mixed results but already support the idea that continuous binge drinking impairs cognitive functioning in young adults (Montgomery et al . ; Stock & Beste ). However, none of the aforementioned studies did explore whether there are already effects of low‐level alcohol use in adolescence.…”

Section: Introductionmentioning

confidence: 99%

Low‐level alcohol consumption during adolescence and its impact on cognitive control development

et al. 2016

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Adolescence is a critical period for maturation of cognitive control and most adolescents start experimenting with alcohol around that time. On the one hand, recent studies indicate that low control abilities predict future problematic alcohol use. On the other hand, binge drinking during young adulthood can (further) impair cognitive control. However, so far no study examined the effects of low-level alcohol use during adolescence. In the present longitudinal fMRI study, we therefore investigated the development of cognitive control in a community-based sample of 92 adolescents at ages 14, 16 and 18. Two different cognitive control functions, i.e. inhibition of pre-potent responses (operationalized by incongruence effects) and switching between different task sets, were measured within one task. Alcohol use in our sample was low (mean: 54 g/week at age 18). The study revealed that neither behavioural nor neural measures of cognitive control function at age 14 predicted alcohol use at age 18 but confirmed established predictors such as gender and personality. As expected, from age 14 to 18, cognitive control abilities were improving (decreased reaction times and/or errors), and activation of cognitive control networks (dorsal anterior cingulate cortex and pre-supplementary motor area) during incongruent trials increased. Unexpectedly, higher alcohol consumption during adolescence was associated with a more pronounced increase in cognitive performance and a smaller increase of neural activation when incongruent trials afforded inhibitory control. We conclude that low-level alcohol use during adolescence does not severely impair ongoing maturation of cognitive control abilities and networks.

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Binge drinking and the differential influence of ethanol on cognitive control subprocesses: a novel field of neurotoxicology

Cited by 9 publications

References 13 publications

Acute Alcohol Effects on Response Inhibition Depend on Response Automatization, but not on GABA or Glutamate Levels in the ACC and Striatum

Acute Alcohol Effects on Response Inhibition Depend on Response Automatization, but not on GABA or Glutamate Levels in the ACC and Striatum

Effects of high‐dose ethanol intoxication and hangover on cognitive flexibility

Low‐level alcohol consumption during adolescence and its impact on cognitive control development

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