Stop-Signal Reaction-Time Task Performance: Role of Prefrontal Cortex and Subthalamic Nucleus

The stop-signal reaction-time (SSRT) task measures inhibition of a response that has already been initiated, that is, the ability to stop. Human subjects classified as “impulsive,” for example, those with attention deficit and hyperactivity disorder, are slower to respond to the stop signal. Althoug...

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Published inCerebral cortex (New York, N.Y. 1991) Vol. 18; no. 1; pp. 178 - 188
Main Authors Eagle, Dawn M., Baunez, Christelle, Hutcheson, Daniel M., Lehmann, Olivia, Shah, Aarti P., Robbins, Trevor W.
Format Journal Article
LanguageEnglish
Published United States Oxford University Press 01.01.2008
Oxford Publishing Limited (England)
Oxford University Press (OUP)
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Summary:The stop-signal reaction-time (SSRT) task measures inhibition of a response that has already been initiated, that is, the ability to stop. Human subjects classified as “impulsive,” for example, those with attention deficit and hyperactivity disorder, are slower to respond to the stop signal. Although functional and structural imaging studies in humans have implicated frontal and basal ganglia circuitry in the mediation of this form of response control, the precise roles of the cortex and basal ganglia in SSRT performance are far from understood. We describe effects of excitotoxic fiber-sparing lesions of the orbitofrontal cortex (OF), infralimbic cortex (IL), and subthalamic nucleus (STN) in rats performing a SSRT task. Lesions to the OF slowed SSRT, whereas lesions to the IL or the STN had no effect. On the go-signal trials, neither cortical lesion affected go-trial reaction time (GoRT), but STN lesions speeded such latencies. The STN lesion also significantly reduced accuracy of stopping at all stop-signal delays, indicative of a generalized stopping impairment that was independent of the SSRT itself.
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ISSN:1047-3211
1460-2199
1460-2199
DOI:10.1093/cercor/bhm044