Locomotor hyperactivity triggered by psychotomimetic drugs like amphetamine and phencyclidine is often linked to dopamine and NMDA receptors, but their pharmacological profiles are more complex. In 32 rats, pre-treatment with haloperidol (dopamine antagonist) or prazosin (noradrenaline antagonist) reduced amphetamine-induced hyperactivity, while ritanserin (serotonin antagonist) had only a partial effect. None of these pre-treatments significantly altered phencyclidine-induced hyperactivity. The findings indicate that both noradrenergic and dopaminergic systems are critical for amphetamine's effects, whereas phencyclidine's hyperlocomotion likely depends on NMDA receptor antagonism. This helps interpret drug-induced hyperactivity as a model of psychosis.
Acute amphetamine caused greater distance traveled (locomotor hyperactivity) in female rats than in male rats, while phencyclidine-induced locomotor hyperactivity was similar in both sexes. No sex differences were observed in amphetamine- or phencyclidine-induced disruption of prepulse inhibition. Male rats showed an increased startle response after amphetamine. These findings suggest that sensitivity to amphetamine, but not phencyclidine, differs between male and female rats, and this sex difference is selective to locomotor hyperactivity and startle, not prepulse inhibition.