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Inhibitory behavioral control: A stochastic dynamic causal modeling study comparing cocaine dependent subjects and controls.

NeuroImage. Clinical | 2015

Cocaine dependence is associated with increased impulsivity in humans. Both cocaine dependence and impulsive behavior are under the regulatory control of cortico-striatal networks. One behavioral laboratory measure of impulsivity is response inhibition (ability to withhold a prepotent response) in which altered patterns of regional brain activation during executive tasks in service of normal performance are frequently found in cocaine dependent (CD) subjects studied with functional magnetic resonance imaging (fMRI). However, little is known about aberrations in specific directional neuronal connectivity in CD subjects. The present study employed fMRI-based dynamic causal modeling (DCM) to study the effective (directional) neuronal connectivity associated with response inhibition in CD subjects, elicited under performance of a Go/NoGo task with two levels of NoGo difficulty (Easy and Hard). The performance on the Go/NoGo task was not significantly different between CD subjects and controls. The DCM analysis revealed that prefrontal-striatal connectivity was modulated (influenced) during the NoGo conditions for both groups. The effective connectivity from left (L) anterior cingulate cortex (ACC) to L caudate was similarly modulated during the Easy NoGo condition for both groups. During the Hard NoGo condition in controls, the effective connectivity from right (R) dorsolateral prefrontal cortex (DLPFC) to L caudate became more positive, and the effective connectivity from R ventrolateral prefrontal cortex (VLPFC) to L caudate became more negative. In CD subjects, the effective connectivity from L ACC to L caudate became more negative during the Hard NoGo conditions. These results indicate that during Hard NoGo trials in CD subjects, the ACC rather than DLPFC or VLPFC influenced caudate during response inhibition.

Pubmed ID: 26082893 RIS Download

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Associated grants

  • Agency: NIDA NIH HHS, United States
    Id: P50DA033935
  • Agency: NCRR NIH HHS, United States
    Id: S10 RR019186
  • Agency: NCRR NIH HHS, United States
    Id: 1 S10 RR019186-01
  • Agency: NIDA NIH HHS, United States
    Id: P20 DA024157
  • Agency: NIDA NIH HHS, United States
    Id: P50 DA009262
  • Agency: NIDA NIH HHS, United States
    Id: P50 DA018197
  • Agency: NIDA NIH HHS, United States
    Id: P50 DA033935
  • Agency: NIDA NIH HHS, United States
    Id: T32 DA007287
  • Agency: NIDA NIH HHS, United States
    Id: U54 DA038999
  • Agency: NIDA NIH HHS, United States
    Id: K05 DA020087
  • Agency: NIDA NIH HHS, United States
    Id: R01 DA034131

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