This chapter provides an overview on exposure to methylazoxymethanol (MAM) at embryonic day 17 as a promising animal model for schizophrenia that mimics behavioral abnormalities and deficits in prefrontal cortex networks. This early insult produces in adult offspring from E17 MAM-treated dams the following: (1) behavioral changes including spontaneous hyperactivity and hypersensitivity to psychotomimetic drugs that are reminiscent of positive symptoms of schizophrenia and associated with a temporal pattern of expression; (2) impaired social interaction similar to that observed in schizophrenic patients existing prior to the onset of disease; (3) cognitive deficits in a variety of domain: working and reference memory, behavioral flexibility, attentional functioning, object recognition, and reversal learning; (4) behavioral abnormalities resembling schizophrenia-related endophenotypes like deficient sensorimotor gating and disrupted latent inhibition; (5) anatomical changes with cortical, thalamic, and hippocampal reductions in volume that are associated with an enlargement of the lateral ventricles; and (6) abnormalities in functional connectivity between brain areas that involve deficits in dopamine, glutamate, and GABA systems. The E17 MAM model that incorporates neuropathological and functional manifestations associated with schizophrenia may help forward early preventive interventions that can successfully reduce the risk of developing schizophrenia in exposed individuals.