Glutamatergic mechanisms in schizophrenia.

By G. Tsai, J. Coyle. Annual Review of Pharmacology and Toxicology, 2003

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The role of glutamate transporters in neurodegenerative diseases and potential opportunities for intervention. (2007, background): “Decreased glutamatergic signaling in prefrontal cortex has been hypothesized to contribute to schizophrenia, possibly through changes in glutamate receptors (Tsai and Coyle, 2002).”
Animal models of schizophrenia (2011, background): “PCP models of schizophrenia In recent years, increasing evidence supports the idea that dysfunction of the glutamatergic system is a primary pathophysiological change seen in schizophrenia (see Olney and Farber, 1995; Tsai and Coyle, 2002; Coyle et al., 2003; Konradi and Heckers, 2003).”
NMDA receptor subunits: function and pharmacology. (2007, background): “PCP or ketamine) disrupt memory formation and cause a schizophrenia-like syndrome in humans, recapitulating both positive and negative symptoms and cognitive impairments [50].”
Abnormal Neural Synchrony in Schizophrenia (2003, background): “Also, given the evidence for NMDA receptor dysregulation in schizophrenia (Javitt and Zukin, 1991; Tsai and Coyle, 2002), another possibility is that abnormalities in pyramidal cells (Lewis and GonzalezBurgos, 2000) could impair the NMDA-mediated glutamate projections from pyramidal cells to interne”