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An Activation Threshold Model for Response Inhibition
Reactive response inhibition (RI) is the cancellation of a prepared response when it is no longer appropriate. Selectivity of RI can be examined by cueing the cancellation of one component of a prepared multi-component response. This substantially delays execution of other components. There is debat...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5235378/ https://www.ncbi.nlm.nih.gov/pubmed/28085907 http://dx.doi.org/10.1371/journal.pone.0169320 |
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author | MacDonald, Hayley J. McMorland, Angus J. C. Stinear, Cathy M. Coxon, James P. Byblow, Winston D. |
author_facet | MacDonald, Hayley J. McMorland, Angus J. C. Stinear, Cathy M. Coxon, James P. Byblow, Winston D. |
author_sort | MacDonald, Hayley J. |
collection | PubMed |
description | Reactive response inhibition (RI) is the cancellation of a prepared response when it is no longer appropriate. Selectivity of RI can be examined by cueing the cancellation of one component of a prepared multi-component response. This substantially delays execution of other components. There is debate regarding whether this response delay is due to a selective neural mechanism. Here we propose a computational activation threshold model (ATM) and test it against a classical “horse-race” model using behavioural and neurophysiological data from partial RI experiments. The models comprise both facilitatory and inhibitory processes that compete upstream of motor output regions. Summary statistics (means and standard deviations) of predicted muscular and neurophysiological data were fit in both models to equivalent experimental measures by minimizing a Pearson Chi-square statistic. The ATM best captured behavioural and neurophysiological dynamics of partial RI. The ATM demonstrated that the observed modulation of corticomotor excitability during partial RI can be explained by nonselective inhibition of the prepared response. The inhibition raised the activation threshold to a level that could not be reached by the original response. This was necessarily followed by an additional phase of facilitation representing a secondary activation process in order to reach the new inhibition threshold and initiate the executed component of the response. The ATM offers a mechanistic description of the neural events underlying RI, in which partial movement cancellation results from a nonselective inhibitory event followed by subsequent initiation of a new response. The ATM provides a framework for considering and exploring the neuroanatomical constraints that underlie RI. |
format | Online Article Text |
id | pubmed-5235378 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-52353782017-02-06 An Activation Threshold Model for Response Inhibition MacDonald, Hayley J. McMorland, Angus J. C. Stinear, Cathy M. Coxon, James P. Byblow, Winston D. PLoS One Research Article Reactive response inhibition (RI) is the cancellation of a prepared response when it is no longer appropriate. Selectivity of RI can be examined by cueing the cancellation of one component of a prepared multi-component response. This substantially delays execution of other components. There is debate regarding whether this response delay is due to a selective neural mechanism. Here we propose a computational activation threshold model (ATM) and test it against a classical “horse-race” model using behavioural and neurophysiological data from partial RI experiments. The models comprise both facilitatory and inhibitory processes that compete upstream of motor output regions. Summary statistics (means and standard deviations) of predicted muscular and neurophysiological data were fit in both models to equivalent experimental measures by minimizing a Pearson Chi-square statistic. The ATM best captured behavioural and neurophysiological dynamics of partial RI. The ATM demonstrated that the observed modulation of corticomotor excitability during partial RI can be explained by nonselective inhibition of the prepared response. The inhibition raised the activation threshold to a level that could not be reached by the original response. This was necessarily followed by an additional phase of facilitation representing a secondary activation process in order to reach the new inhibition threshold and initiate the executed component of the response. The ATM offers a mechanistic description of the neural events underlying RI, in which partial movement cancellation results from a nonselective inhibitory event followed by subsequent initiation of a new response. The ATM provides a framework for considering and exploring the neuroanatomical constraints that underlie RI. Public Library of Science 2017-01-13 /pmc/articles/PMC5235378/ /pubmed/28085907 http://dx.doi.org/10.1371/journal.pone.0169320 Text en © 2017 MacDonald et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article MacDonald, Hayley J. McMorland, Angus J. C. Stinear, Cathy M. Coxon, James P. Byblow, Winston D. An Activation Threshold Model for Response Inhibition |
title | An Activation Threshold Model for Response Inhibition |
title_full | An Activation Threshold Model for Response Inhibition |
title_fullStr | An Activation Threshold Model for Response Inhibition |
title_full_unstemmed | An Activation Threshold Model for Response Inhibition |
title_short | An Activation Threshold Model for Response Inhibition |
title_sort | activation threshold model for response inhibition |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5235378/ https://www.ncbi.nlm.nih.gov/pubmed/28085907 http://dx.doi.org/10.1371/journal.pone.0169320 |
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