Abstract
N-methyl-D-aspartate receptor (NMDAR) hypofunction has been implicated in the pathophysiology of schizophrenia and its associated cognitive impairments, including auditory processing deficits reflected by the P300 event-related potential (ERP) component. P300 amplitude reduction is one of the most widely replicated brain abnormalities observed in patients with schizophrenia. To test the hypothesized contribution of NMDAR hypofunction to P300 abnormalities, we examined the effects of the NMDAR antagonist ketamine on auditory P300 amplitudes in healthy individuals and compared these effects with those of schizophrenia.
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