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.