Current treatments for schizophrenia, including both typical and atypical antipsychotics, function primarily by blocking dopamine (D2) receptors. While effective for treatment of positive symptoms, antipsychotics have limited efficacy against persistent negative symptoms or cognitive impairments, necessitating the development of alternative treatment approaches. Recent neurochemical models of persistent dysfunction focus on disturbances of brain glutamatergic (NMDAR) neurotransmission. Mechanisms by which NMDAR dysfunction leads to symptoms, however, remain relatively unexplored. As opposed to dopaminergic models, glutamatergic models specifically account for impairments not only in cognition, but also in the generation of neurophysiological measures, such as visual P1 or auditory mismatch (MMN). Such measures index local circuit dysfunction, and thus may be useful as translational biomarkers for translational drug development.