Unilateral nigrostriatal dopamine depletion in animals induces contralateral sensorimotor deficits that are like symptoms associated with Parkinson's disease (PD). Unilateral nigrostriatal dopamine depletion also causes a contralateral deficit in disengagement behavior (e.g., ability to stop an ongoing activity to orient/attend to a new stimulus). This disengagement deficit has been shown to be resistant to treatments that rescued other motor and somatosensory deficits. Thus, disengagement behavior may involve unique sensorimotor information integration potentially important for attentional allocation and may rely strongly on a mechanism that includes extranigrostriatal circuitry. The central nucleus of the amygdala (CeA) and its connections with the nigral dopamine system have been reported to modulate cognitive processes dependent substantially on attentional allocation. CeA dopamine function might be also important for disengagement behavior. In Experiment 1, rats received microinfusions of 6-hydroxydopamine unilaterally to induce dopamine terminal loss in the CeA and were tested for disengagement behavior in addition to several sensorimotor functions. These rats showed deficits in contralateral disengagement behavior and an asymmetry in adhesive dot removal from the paws, but not in forelimb use in a cylinder or amphetamine rotation. In Experiment 2, rats received D1 or D2 antagonists into the CeA unilaterally prior to behavioral tests. The D1 antagonist disrupted disengagement behavior without affecting the other sensorimotor tests examined. The D2 antagonist had no effects on any of the behaviors tested. Our results suggest that CeA dopamine function is involved in modulation of disengagement behavior.