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Rigid reduced successor representation as a potential mechanism for addiction
Difficulty in cessation of drinking, smoking, or gambling has been widely recognized. Conventional theories proposed relative dominance of habitual over goal‐directed control, but human studies have not convincingly supported them. Referring to the recently suggested “successor representation (SR)”...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8252639/ https://www.ncbi.nlm.nih.gov/pubmed/33840120 http://dx.doi.org/10.1111/ejn.15227 |
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author | Shimomura, Kanji Kato, Ayaka Morita, Kenji |
author_facet | Shimomura, Kanji Kato, Ayaka Morita, Kenji |
author_sort | Shimomura, Kanji |
collection | PubMed |
description | Difficulty in cessation of drinking, smoking, or gambling has been widely recognized. Conventional theories proposed relative dominance of habitual over goal‐directed control, but human studies have not convincingly supported them. Referring to the recently suggested “successor representation (SR)” of states that enables partially goal‐directed control, we propose a dopamine‐related mechanism that makes resistance to habitual reward‐obtaining particularly difficult. We considered that long‐standing behavior towards a certain reward without resisting temptation can (but not always) lead to a formation of rigid dimension‐reduced SR based on the goal state, which cannot be updated. Then, in our model assuming such rigid reduced SR, whereas no reward prediction error (RPE) is generated at the goal while no resistance is made, a sustained large positive RPE is generated upon goal reaching once the person starts resisting temptation. Such sustained RPE is somewhat similar to the hypothesized sustained fictitious RPE caused by drug‐induced dopamine. In contrast, if rigid reduced SR is not formed and states are represented individually as in simple reinforcement learning models, no sustained RPE is generated at the goal. Formation of rigid reduced SR also attenuates the resistance‐dependent decrease in the value of the cue for behavior, makes subsequent introduction of punishment after the goal ineffective, and potentially enhances the propensity of nonresistance through the influence of RPEs via the spiral striatum‐midbrain circuit. These results suggest that formation of rigid reduced SR makes cessation of habitual reward‐obtaining particularly difficult and can thus be a mechanism for addiction, common to substance and nonsubstance reward. |
format | Online Article Text |
id | pubmed-8252639 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82526392021-07-12 Rigid reduced successor representation as a potential mechanism for addiction Shimomura, Kanji Kato, Ayaka Morita, Kenji Eur J Neurosci Clinical and Translational Neuroscience Difficulty in cessation of drinking, smoking, or gambling has been widely recognized. Conventional theories proposed relative dominance of habitual over goal‐directed control, but human studies have not convincingly supported them. Referring to the recently suggested “successor representation (SR)” of states that enables partially goal‐directed control, we propose a dopamine‐related mechanism that makes resistance to habitual reward‐obtaining particularly difficult. We considered that long‐standing behavior towards a certain reward without resisting temptation can (but not always) lead to a formation of rigid dimension‐reduced SR based on the goal state, which cannot be updated. Then, in our model assuming such rigid reduced SR, whereas no reward prediction error (RPE) is generated at the goal while no resistance is made, a sustained large positive RPE is generated upon goal reaching once the person starts resisting temptation. Such sustained RPE is somewhat similar to the hypothesized sustained fictitious RPE caused by drug‐induced dopamine. In contrast, if rigid reduced SR is not formed and states are represented individually as in simple reinforcement learning models, no sustained RPE is generated at the goal. Formation of rigid reduced SR also attenuates the resistance‐dependent decrease in the value of the cue for behavior, makes subsequent introduction of punishment after the goal ineffective, and potentially enhances the propensity of nonresistance through the influence of RPEs via the spiral striatum‐midbrain circuit. These results suggest that formation of rigid reduced SR makes cessation of habitual reward‐obtaining particularly difficult and can thus be a mechanism for addiction, common to substance and nonsubstance reward. John Wiley and Sons Inc. 2021-05-10 2021-06 /pmc/articles/PMC8252639/ /pubmed/33840120 http://dx.doi.org/10.1111/ejn.15227 Text en © 2021 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd. 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 | Clinical and Translational Neuroscience Shimomura, Kanji Kato, Ayaka Morita, Kenji Rigid reduced successor representation as a potential mechanism for addiction |
title | Rigid reduced successor representation as a potential mechanism for addiction |
title_full | Rigid reduced successor representation as a potential mechanism for addiction |
title_fullStr | Rigid reduced successor representation as a potential mechanism for addiction |
title_full_unstemmed | Rigid reduced successor representation as a potential mechanism for addiction |
title_short | Rigid reduced successor representation as a potential mechanism for addiction |
title_sort | rigid reduced successor representation as a potential mechanism for addiction |
topic | Clinical and Translational Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8252639/ https://www.ncbi.nlm.nih.gov/pubmed/33840120 http://dx.doi.org/10.1111/ejn.15227 |
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