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The Journal of Neuroscience, August 12, 2009, 29(32):10171-10179; doi:10.1523/JNEUROSCI.1300-09.2009

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Behavioral/Systems/Cognitive
Functional Connectivity Delineates Distinct Roles of the Inferior Frontal Cortex and Presupplementary Motor Area in Stop Signal Inhibition

Jeng-Ren Duann,¹ Jaime S. Ide,² Xi Luo,^2,3 and Chiang-shan Ray Li^2,4,5

¹Swartz Center for Computational Neuroscience, Institute of Neural Computation, University of California, San Diego, San Diego, California 92093, and Departments of ²Psychiatry, ³Statistics, and ⁴Neurobiology and ⁵Interdepartmental Neuroscience Program, Yale University, New Haven, Connecticut 06519

Correspondence should be addressed to Dr. Chiang-shan Ray Li, Connecticut Mental Health Center, S103, Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT 06519. Email: chiang-shan.li{at}yale.edu

The neural basis of motor response inhibition has drawn considerable attention in recent imaging literature. Many studies have used the go/no-go or stop signal task to examine the neural processes underlying motor response inhibition. In particular, showing greater activity during no-go (stop) compared with go trials and during stop success compared with stop error trials, the right inferior prefrontal cortex (IFC) has been suggested by numerous studies as the cortical area mediating response inhibition. Many of these same studies as well as others have also implicated the presupplementary motor area (preSMA) in this process, in accord with a function of the medial prefrontal cortex in goal-directed action. Here we used connectivity analyses to delineate the roles of IFC and preSMA during stop signal inhibition. Specifically, we hypothesized that, as an integral part of the ventral attention system, the IFC responds to a stop signal and expedites the stop process in the preSMA, the primary site of motor response inhibition. This hypothesis predicted that preSMA and primary motor cortex would show functional interconnectivity via the basal ganglia circuitry to mediate response execution or inhibition, whereas the IFC would influence the basal ganglia circuitry via connectivity with preSMA. The results of Granger causality analyses in 57 participants confirmed this hypothesis. Furthermore, psychophysiological interaction showed that, compared with stop errors, stop successes evoked greater effective connectivity between the IFC and preSMA, providing additional support for this hypothesis. These new findings provided evidence critically differentiating the roles of IFC and preSMA during stop signal inhibition and have important implications for our understanding of the component processes of inhibitory control.

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Received March 17, 2009; revised July 6, 2009; accepted July 11, 2009.

Correspondence should be addressed to Dr. Chiang-shan Ray Li, Connecticut Mental Health Center, S103, Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT 06519. Email: chiang-shan.li{at}yale.edu

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