The motor-activating effects of amphetamine and other psychostimulants such as cocaine depend on an increase in dopamine (DA) transmission in the striatum, a key component of the basal ganglia and the forebrain motive circuit. This review focuses on research aimed at using electrophysiological techniques--including extracellular unit recording and iontophoresis--in alert, fully functioning animals to understand how these drugs alter striatal neuronal processing under behaviorally relevant conditions. The data indicate that DA works in conjunction with glutamate (GLU), an excitatory amino acid, to enhance the signal-to-noise ratio of afferent information. This DA-GLU interaction appears to play a critical role in the amphetamine-induced activation of striatal neurons. The pattern of striatal activation, moreover, changes as the behavioral response changes from unfocused locomotion to highly focused, stereotyped behavior, but interestingly, the striatal response pattern is not reflected in substantia nigra reticulata, a primary target of striatal efferents. Although cocaine also activates striatal neurons during behavior, the underlying mechanisms appear to be complicated by factors unique to this drug and deserve further evaluation. Collectively, these findings provide unique insight into the neuronal processes by which the striatum participates in psychostimulant-induced motor behavior.