The motor depressant effects of caerulein and N-propylnorapomorphine (NPA) were compared in male mice. Caerulein (1-50 micrograms/kg SC) in a dose dependent manner depressed the exploratory activity, whereas NPA in lower doses (0.5-10 micrograms/kg SC) decreased the motor activity, but in higher doses (over 50 micrograms/kg) had stimulating effect on the exploratory behavior. In mice selected according to their motor response after administration of 100 micrograms/kg NPA to weak and strong responders, the low dose of NPA (1 microgram/kg) similarly suppressed motor activity in both selected groups, while the effect of caerulein (2 micrograms/kg) was apparently higher in weak responders. Destruction of catecholaminergic terminals by 6-hydroxydopamine (60 micrograms ICV) reversed completely the motor depressant effect of NPA, whereas degeneration of serotoninergic terminals (5,7-dihydroxytryptamine 60 micrograms ICV or p-chloroamphetamine 2 X 15 mg/kg IP) enhanced the sedative effect of NPA. The motor depressant effect of caerulein remained unchanged after lesions of monoaminergic terminals in forebrain. Subchronic haloperidol (0.25 mg/kg IP, twice daily during 14 days) treatment, reducing significantly the density of high-affinity dopamine2- and serotonin2-receptors, decreased the motor depressant action of caerulein. It is possible that motor depressant effect of caerulein, differently from the action of NPA, is mediated through the high-affinity dopamine2-receptors and in lesser extent through the high-affinity serotonin2-receptors.