Several different classes of pharmacological agents produce syndromes of behavioral activation in humans and infrahumans. While many of these agents, including direct and indirect sympathomimetics, methylxanthines, opiates and several neuropeptides have very distinct neurochemical profiles, it is not clear whether their behavioral stimulant action results from their action on a common neural substrate, or instead from their action on parallel but separate activation "circuits.' Using photocell measurements of motor activity in rats, it has been possible to demonstrate that some agents with very distinct neurochemical identities act on common neural substrates to produce behavioral activation, while other agents act on completely distinct brain regions. Specifically, the locomotor-activating properties of direct and indirect sympathomimetics and opiates appear to result from their action within the basal ganglia, including the ventral striatum and globus pallidus, while the activating properties of caffeine and the neuropeptide, corticotropin releasing factor (CRF) appear to be independent of this circuitry. These findings suggest the presence of at least two separate neural systems capable of mediating behavioral activation.