Recent evidence indicates that neuroactive steroids may participate in the pathogenesis of schizophrenia spectrum disorders, yet the mechanisms of this involvement are elusive. As 5-α-reductase (5AR) is the rate-limiting enzyme of one of the two major metabolic pathways in brain steroidogenesis, we investigated the effects of its blockade in several rat models of psychotic-like behavior. The 5AR inhibitor finasteride (FIN, 60 or 100 mg/kg, intraperitoneal, ip) dose-and time-dependently antagonized prepulse inhibition (PPI) deficits induced by apomorphine (APO, 0.25 mg/kg, subcutaneous, sc) and d-amphetamine (AMPH, 5 mg/kg, sc), in a manner analogous to haloperidol (HAL, 0.1 mg/kg, ip) and clozapine (CLO, 5 mg/kg, ip). Similar results were observed with the other 5AR inhibitors dutasteride (DUT, 40 or 80 mg/kg, ip) and SKF 105111 (30 mg/kg, ip). FIN (60 or 100 mg/kg, ip) also reduced hyperlocomotion induced by AMPH (1 or 3 mg/kg, sc) and attenuated stereotyped behaviors induced by APO (0.25 mg/kg, sc). Nevertheless, FIN (100 mg/kg, ip) did not reverse the PPI disruption induced by the N-methyl-d-aspartate receptor antagonist dizocilpine (0.1 mg/kg, sc). FIN (60–300 mg/kg, ip) induced no catalepsy in either the bar test or the paw test. Our results suggest that 5AR inhibitors elicit antipsychotic-like effects in animals and may be proposed as a putative novel target in the management of psychotic disorders.