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At‐risk alcohol users have disrupted valence discrimination during reward anticipation

Alcohol use disorder is characterised by disrupted reward learning, underpinned by dysfunctional cortico‐striatal reward pathways, although relatively little is known about the biology of reward processing in populations who engage in risky alcohol use. Cues that trigger reward anticipation can be c...

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Autores principales: Komarnyckyj, Mica, Retzler, Chris, Cao, Zhipeng, Ganis, Giorgio, Murphy, Anna, Whelan, Robert, Fouragnan, Elsa Florence
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9286798/
https://www.ncbi.nlm.nih.gov/pubmed/35470555
http://dx.doi.org/10.1111/adb.13174
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author Komarnyckyj, Mica
Retzler, Chris
Cao, Zhipeng
Ganis, Giorgio
Murphy, Anna
Whelan, Robert
Fouragnan, Elsa Florence
author_facet Komarnyckyj, Mica
Retzler, Chris
Cao, Zhipeng
Ganis, Giorgio
Murphy, Anna
Whelan, Robert
Fouragnan, Elsa Florence
author_sort Komarnyckyj, Mica
collection PubMed
description Alcohol use disorder is characterised by disrupted reward learning, underpinned by dysfunctional cortico‐striatal reward pathways, although relatively little is known about the biology of reward processing in populations who engage in risky alcohol use. Cues that trigger reward anticipation can be categorized according to their learnt valence (i.e., positive vs. negative outcomes) and motivational salience (i.e., incentive vs. neutral cues). Separating EEG signals associated with these dimensions is challenging because of their inherent collinearity, but the recent application of machine learning methods to single EEG trials affords a solution. Here, the Alcohol Use Disorders Identification Test (AUDIT) was used to quantify risky alcohol use, with participants split into high alcohol (HA) (n = 22, mean AUDIT score: 13.82) and low alcohol (LA) (n = 22, mean AUDIT score: 5.77) groups. We applied machine learning multivariate single‐trial classification to the electroencephalography (EEG) data collected during reward anticipation. The LA group demonstrated significant valence discrimination in the early stages of reward anticipation within the cue‐P3 time window (400–550 ms), whereas the HA group was insensitive to valence within this time window. Notably, the LA, but not the HA group demonstrated a relationship between single‐trial variability in the early valence component and reaction times for gain and loss trials. This study evidences disrupted hypoactive valence sensitivity in the HA group, revealing potential neurophysiological markers for risky drinking behaviours which place individuals at‐risk of adverse health events.
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spelling pubmed-92867982022-07-19 At‐risk alcohol users have disrupted valence discrimination during reward anticipation Komarnyckyj, Mica Retzler, Chris Cao, Zhipeng Ganis, Giorgio Murphy, Anna Whelan, Robert Fouragnan, Elsa Florence Addict Biol Original Articles Alcohol use disorder is characterised by disrupted reward learning, underpinned by dysfunctional cortico‐striatal reward pathways, although relatively little is known about the biology of reward processing in populations who engage in risky alcohol use. Cues that trigger reward anticipation can be categorized according to their learnt valence (i.e., positive vs. negative outcomes) and motivational salience (i.e., incentive vs. neutral cues). Separating EEG signals associated with these dimensions is challenging because of their inherent collinearity, but the recent application of machine learning methods to single EEG trials affords a solution. Here, the Alcohol Use Disorders Identification Test (AUDIT) was used to quantify risky alcohol use, with participants split into high alcohol (HA) (n = 22, mean AUDIT score: 13.82) and low alcohol (LA) (n = 22, mean AUDIT score: 5.77) groups. We applied machine learning multivariate single‐trial classification to the electroencephalography (EEG) data collected during reward anticipation. The LA group demonstrated significant valence discrimination in the early stages of reward anticipation within the cue‐P3 time window (400–550 ms), whereas the HA group was insensitive to valence within this time window. Notably, the LA, but not the HA group demonstrated a relationship between single‐trial variability in the early valence component and reaction times for gain and loss trials. This study evidences disrupted hypoactive valence sensitivity in the HA group, revealing potential neurophysiological markers for risky drinking behaviours which place individuals at‐risk of adverse health events. John Wiley and Sons Inc. 2022-04-07 2022-05 /pmc/articles/PMC9286798/ /pubmed/35470555 http://dx.doi.org/10.1111/adb.13174 Text en © 2022 The Authors. Addiction Biology published by John Wiley & Sons Ltd on behalf of Society for the Study of Addiction. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Komarnyckyj, Mica
Retzler, Chris
Cao, Zhipeng
Ganis, Giorgio
Murphy, Anna
Whelan, Robert
Fouragnan, Elsa Florence
At‐risk alcohol users have disrupted valence discrimination during reward anticipation
title At‐risk alcohol users have disrupted valence discrimination during reward anticipation
title_full At‐risk alcohol users have disrupted valence discrimination during reward anticipation
title_fullStr At‐risk alcohol users have disrupted valence discrimination during reward anticipation
title_full_unstemmed At‐risk alcohol users have disrupted valence discrimination during reward anticipation
title_short At‐risk alcohol users have disrupted valence discrimination during reward anticipation
title_sort at‐risk alcohol users have disrupted valence discrimination during reward anticipation
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9286798/
https://www.ncbi.nlm.nih.gov/pubmed/35470555
http://dx.doi.org/10.1111/adb.13174
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