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Effects of binge drinking on action cascading processes: an EEG study

  • Organ Toxicity and Mechanisms
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Abstract

High-dosage alcohol intoxication (i.e., binge drinking in humans) is an increasingly prevalent problem. Despite the well-known long-term consequences, the acute effects of high-dosage alcohol intoxication on cognitive control processes have not been investigated with respect to neurophysiological changes in humans. We provide insights into the effects of high-dosage ethanol intoxication on action control functions in humans on the basis of neurophysiological (EEG) data. Action control processes were examined in a stop–change task. Based on a detailed analysis of behavioral and electrophysiological data, we demonstrate a specific modulation of action cascading processes. Opposed to commonly held views, high-dosage ethanol intoxication (0.9–1.13 ‰) exerts highly specific effects on cognitive subprocesses mediating action control. If action control processes are performed in succession, intoxicated and non-intoxicated participants perform equally well. However, action control processes become compromised during high-dosage ethanol intoxication, when different response options require processing resources in parallel. Under high-dose ethanol intoxication, subjects are not able to prioritize different response options. We could demonstrate that the effects were of high effect sizes (η 2 = 0.702) and rely more on response selection deficits than on deficits in attentional processing. The changes in response selection processes are mediated via the anterior cingulate cortex. The specificity of the observed effects may be due to a differential involvement of dopaminergic and GABAergic processes in action control and attentional selection processes.

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Notes

  1. One limitation to this interpretation remains: According to Verbruggen et al. (2008), it is impossible to distinguish between the behavioral effects (RT slope values) of a nondeterministic serial processes and parallel processing based on the RT slope value (c.f. Verbruggen et al. 2008 for a detailed discussion on this issue).

  2. The (Nogo)-N2 (occurring 200–300 ms after the inhibitory signal, see e.g. van Boxtel et al. 2001; Falkenstein et al. 1999) has frequently been analyzed with respect to inhibitory control processes. In the SC trials, a Nogo-N2 like component is evident in the SCD 300 condition (refer Fig. 4). However, in the SCD 0 condition, this component is not detectable due to the simultaneously occurring change processes. Since the (Nogo)-N2 is thus not quantifiable in all conditions, the (Nogo)-N2 was not included in the analyses.

  3. We run an analysis where we included the factor “time” (first or second session with alcohol intoxication) as a between-subject factor in the ANOVA. There was no main effect “time” and no interaction effect with this factor in the behavioral and the neurophysiological data (all F < 1.1; p > .3). The results are therefore unbiased with respect to the testing point.

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Acknowledgments

This research was supported by a Grant from the Deutsche Forschungsgemeinschaft (DFG) BE4045/10-1. For the duration of data collection, the breathalyzer “Alcotest 300” was provided by Dräger Safety AG & Co. KGaA.

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Stock, AK., Blaszkewicz, M. & Beste, C. Effects of binge drinking on action cascading processes: an EEG study. Arch Toxicol 88, 475–488 (2014). https://doi.org/10.1007/s00204-013-1109-2

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