Over the past 20 years, attention has turned increasingly to dysfunction of the brain glutamate system as a fundamental underlying pathophysiology in schizophrenia. Attention first turned to glutamatergic systems with the observation that phencyclidine (PCP) and similarly acting psychotomimetic compounds induced their unique behavioral effects by blocking neurotransmission at N-methyl-D-aspartate (NMDA) type glutamate receptors. The glutamatergic hypothesis has since been expanded to include a potential role for dysfunction at other subtypes of glutamatergic receptors, as well as linkages between schizophrenia and glutamate receptor genes. Moreover, accumulating evidence supports a link between the NMDA system, disordered cognition, and sensory (auditory and visual) processing.
