Identification of functional molecules in the brain related to improvement of motor dysfunction after stroke will contribute to establish a new treatment strategy for stroke rehabilitation. Hence, monoamine changes in basal ganglion related to motor control were examined in groups with/without voluntary exercise after cerebral infarction. Cerebral infarction was produced by photothrombosis in rats. Voluntary exercise using a running wheel was initiated from 2 days after surgery. Motor performance was measured by the accelerated rotarod test. Monoamine concentrations in striatum were analyzed using HPLC and immunohistochemical staining performed with anti-tyrosine hydroxylase antibody. In behavioral evaluation, the mean latency until falling from the rotating rod in the group with exercise (infarction-EX group) was significantly longer than that in the group without exercise (infarction-CNT group). When concerning the alteration of monoamine concentration between before and 2 days after infarction, dopamine level showed a significant increase 2 days after infarction. Subsequently, dopamine level was significantly decreased in the infarction-EX group at 10 days after infarction; in contrast, both norepinephrine and 5-HT concentrations were significantly higher in the infarction-EX group than in the infarction-CNT group. Furthermore, duration of rotarod test showed a significant inverse correlation with dopamine levels and a significant positive correlation with 5-HT levels. In immunohistochemical analysis, tyrosine hydroxylase immunoreactivity in substantia nigra pars compacta was shown to increase in the infarction-CNT group. In the present study, at least some of the alterations of monoamines associated with the improvement of paralysis in the basal ganglion related to motor control might have been detected.