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Switch costs in inhibitory control and voluntary behaviour: A computational study of the antisaccade task


Aponte, Eduardo A; Stephan, Klaas E; Heinzle, Jakob (2019). Switch costs in inhibitory control and voluntary behaviour: A computational study of the antisaccade task. European Journal of Neuroscience, 50(7):3205-3220.

Abstract

An integral aspect of human cognition is the ability to inhibit stimulus-driven, habitual responses, in favour of complex, voluntary actions. In addition, humans can also alternate between different tasks. This comes at the cost of degraded performance when compared to repeating the same task, a phenomenon called the "task-switch cost." While task switching and inhibitory control have been studied extensively, the interaction between them has received relatively little attention. Here, we used the SERIA model, a computational model of antisaccade behaviour, to draw a bridge between them. We investigated task switching in two versions of the mixed antisaccade task, in which participants are cued to saccade either in the same or in the opposite direction to a peripheral stimulus. SERIA revealed that stopping a habitual action leads to increased inhibitory control that persists onto the next trial, independently of the upcoming trial type. Moreover, switching between tasks induces slower and less accurate voluntary responses compared to repeat trials. However, this only occurs when participants lack the time to prepare the correct response. Altogether, SERIA demonstrates that there is a reconfiguration cost associated with switching between voluntary actions. In addition, the enhanced inhibition that follows antisaccade but not prosaccade trials explains asymmetric switch costs. In conclusion, SERIA offers a novel model of task switching that unifies previous theoretical accounts by distinguishing between inhibitory control and voluntary action generation and could help explain similar phenomena in paradigms beyond the antisaccade task.

Abstract

An integral aspect of human cognition is the ability to inhibit stimulus-driven, habitual responses, in favour of complex, voluntary actions. In addition, humans can also alternate between different tasks. This comes at the cost of degraded performance when compared to repeating the same task, a phenomenon called the "task-switch cost." While task switching and inhibitory control have been studied extensively, the interaction between them has received relatively little attention. Here, we used the SERIA model, a computational model of antisaccade behaviour, to draw a bridge between them. We investigated task switching in two versions of the mixed antisaccade task, in which participants are cued to saccade either in the same or in the opposite direction to a peripheral stimulus. SERIA revealed that stopping a habitual action leads to increased inhibitory control that persists onto the next trial, independently of the upcoming trial type. Moreover, switching between tasks induces slower and less accurate voluntary responses compared to repeat trials. However, this only occurs when participants lack the time to prepare the correct response. Altogether, SERIA demonstrates that there is a reconfiguration cost associated with switching between voluntary actions. In addition, the enhanced inhibition that follows antisaccade but not prosaccade trials explains asymmetric switch costs. In conclusion, SERIA offers a novel model of task switching that unifies previous theoretical accounts by distinguishing between inhibitory control and voluntary action generation and could help explain similar phenomena in paradigms beyond the antisaccade task.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Biomedical Engineering
Dewey Decimal Classification:170 Ethics
610 Medicine & health
Scopus Subject Areas:Life Sciences > General Neuroscience
Uncontrolled Keywords:General Neuroscience
Language:English
Date:1 October 2019
Deposited On:30 Jan 2020 10:33
Last Modified:29 Jul 2020 11:50
Publisher:Wiley-Blackwell Publishing, Inc.
ISSN:0953-816X
OA Status:Closed
Publisher DOI:https://doi.org/10.1111/ejn.14435
PubMed ID:31081574

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