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pubmed-article:19508693pubmed:dateCreated2009-7-9lld:pubmed
pubmed-article:19508693pubmed:abstractTextThe ability to perform an appropriate response in the presence of competing alternatives is a critical facet of human behavioral control. This is especially important if a response is prepared for execution but then has to be changed suddenly. A popular hypothesis of basal ganglia (BG) function suggests that its direct and indirect pathways could provide a neural mechanism to rapidly switch from one planned response to an alternative. However, if one response is more dominant or 'automatic' than the other, the BG might have a different role depending on switch direction. We built upon the pro- and antisaccade tasks, two models of automatic and voluntary behavior, respectively, and investigated whether the BG are important for switching any planned response in general, or if they are more important for switching from a more automatic response to a response that is more difficult to perform. Subjects prepared either a pro- or antisaccade but then had to switch it unexpectedly on a subset of trials. The results revealed increased striatal activation for switching from a pro- to an antisaccade but this did not occur for switching from an anti- to a prosaccade. This activation pattern depended on the relative difficulty in switching, and it was distinct from frontal eye fields, an area shown to be more active for antisaccade trials than for prosaccade trials. This suggests that the BG are important for compensating for differences in response difficulty, facilitating the rapid switching of one response for another.lld:pubmed
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pubmed-article:19508693pubmed:year2009lld:pubmed
pubmed-article:19508693pubmed:articleTitleRole of the basal ganglia in switching a planned response.lld:pubmed
pubmed-article:19508693pubmed:affiliationCentre for Neuroscience Studies, 18 Stuart Street, Queen's University, Kingston, Ontario, Canada.lld:pubmed
pubmed-article:19508693pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19508693pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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