Schizophrenia is characterized by delusions, hallucinations, cognitive deficits, and social withdrawal. Emerging evidence links its onset to harmful intrauterine factors, leading to the development of maternal immune activation (MIA) as a relevant experimental model. This study evaluated behavioral alterations and the potential neuroprotective role of melatonin (MEL) in a rat model of schizophrenia induced by MIA. Three groups were established: a) MIA rats, injected with poly I:C acid (10 mg/kg, GD12); b) MIA+MEL, injected with poly I:C and treated with MEL (30 mg/kg, GD12 to two weeks postpartum); and c) Controls, injected with saline. Male offspring were assessed at postnatal day 30 using the open-field and elevated plus maze tests. In the maze, MIA offspring entered open arms less frequently than controls (3±0.60 vs 5.33±0.69; p<0.05), suggesting impaired anxiety regulation; melatonin did not prevent this effect (2.69±0.47). In the open-field, MIA rats showed reduced exploratory behavior, with fewer head dips compared to controls (6.5±2.97 vs 10.7±5.18; p<0.05). Melatonin showed a trend toward improvement (7.93±3.45; p=0.05). These findings suggest that MIA induces measurable anxiety and apathy-like behaviors in offspring. While melatonin did not reverse all alterations, it showed partial benefits in exploratory activity. Further behavioral and neurobiological studies are needed to clarify its preventive potential in schizophrenia-related neurodevelopmental disturbances.