Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia.

ABSTRACT: 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 sch

SUBMITTER: Cabungcal JH 

PROVIDER: S-EPMC4418441 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature