Glutamatergic models provide specific predictions regarding the nature and extent of cognitive dysfunction in schizophrenia that differ from those provided by other types of models. Such predictions have been significantly supported by behavioral, neurophysiological, and neuroimaging-type studies, implicating N-methyl-D-aspartate (NMDA) receptor dysfunction as a key neurobiological determinant of impaired cognition in schizophrenia. Deficits in learning and declarative memory, which localize to the hippocampus, have been extensively documented. Deficits in prefrontal cortex (PFC)/executive processing have been extensively evaluated in schizophrenia, using measures such as Wisconsin Card Sorting Test (WCST), Stroop, N-back, or AX-version of the Continuous Performance Test (AX-CPT). Auditory functions in schizophrenia have been historically understudied, in part because no deficits are observed in simple audiometric screening tests. The NMDA receptors are located at multiple levels of the early visual system, including the retina, lateral geniculate nucleus (LGN), and primary cortex.