Abnormal development can lead to deficits in adult brain function, a trajectory likely underlying adolescent-onset psychiatric conditions such as schizophrenia. Developmental manipulations yielding adult deficits in rodents provide an opportunity to explore mechanisms involved in a delayed emergence of anomalies driven by developmental alterations. Here we assessed whether oxidative stress during presymptomatic stages causes adult anomalies in rats with a neonatal ventral hippocampal lesion, a developmental rodent model useful for schizophrenia research. Juvenile and adolescent treatment with the antioxidant N-acetyl cysteine prevented the reduction of prefrontal parvalbumin interneuron activity observed in this model, as well as electrophysiological and behavioral deficits relevant to schizophrenia. Adolescent treatment with the glutathione peroxidase mimic ebselen also reversed behavioral deficits in this animal model. These findings suggest that presymptomatic oxidative stress yields abnormal adult brain function in a developmentally compromised brain, and highlight redox modulation as a potential target for early intervention. •Presymptomatic antioxidant treatment prevents loss of parvalbumin in NVHL rats•Antioxidant treatment prevents altered prefrontal electrophysiology in NVHL rats•Prepulse inhibition deficits are prevented by antioxidants Cabungcal et al. show that antioxidant treatment during juvenile and adolescent stages prevents the onset of electrophysiological and behavioral deficits in a developmental model for schizophrenia. The reversal of adolescent-onset deficits suggests redox modulation is a potential target for early intervention.