title: Molecular biological investigations into the role of the NMDA receptor in the pathophysiology of schizophrenia.
abstract: OBJECTIVE
  There is increasing acceptance that schizophrenia is associated with a generalised disorder in cortical neurodevelopment. The aim of this paper is to review the evidence that this disorder may be accounted for by abnormalities in mechanisms mediated by the main family of excitatory neuroreceptors in cortical brain systems, the N-methyl-D-aspartate (NMDA) glutamatergic receptors.
  
  
  METHODS
  The neurobiological evidence is presented for an abnormality in cortical development related to synaptic pathology in schizophrenia. The unique functions of the NMDA receptor in information processing are described, especially its role in learning and memory, and in neural plasticity and brain development. It is argued that the cellular and molecular mechanisms which underlie learning and memory also govern normal brain development. Studies examining abnormalities in glutamatergic transmission in schizophrenia are reviewed.
  
  
  RESULTS
  There is a substantial literature in support of the possibility that NMDA receptor abnormalities may be involved in the neurodevelopmental predisposition to schizophrenia, as well as in symptom production.
  
  
  CONCLUSIONS
  Research to determine the role of the NMDA receptor in the pathophysiology of schizophrenia is warranted and now feasible. To be successful, this research will require the application of molecular biology techniques to postmortem brain tissue studies, in addition to traditional histochemical approaches.
authors.affiliation: Psychiatric Unit, Prince of Wales Hospital, Randwick, New South Wales, Australia.
authors.forename: S V
authors.initials: SV
authors.lastname: Catts
authors.forename: P B
authors.initials: PB
authors.lastname: Ward
authors.forename: A
authors.initials: A
authors.lastname: Lloyd
authors.forename: X F
authors.initials: XF
authors.lastname: Huang
authors.forename: G
authors.initials: G
authors.lastname: Dixon
authors.forename: L
authors.initials: L
authors.lastname: Chahl
authors.forename: C
authors.initials: C
authors.lastname: Harper
authors.forename: D
authors.initials: D
authors.lastname: Wakefield
mesh_terms: D002540:Cerebral Cortex / Q000503:physiopathology; D015870:Gene Expression / Q000502:physiology; D006801:Humans; D008967:Molecular Biology; D012333:RNA, Messenger / Q000235:genetics; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics* / Q000502:physiology; D012559:Schizophrenia / Q000235:genetics* / Q000503:physiopathology; D012565:Schizophrenic Psychology; D009435:Synaptic Transmission / Q000235:genetics / Q000502:physiology
chemical_list: D012333:RNA, Messenger; D016194:Receptors, N-Methyl-D-Aspartate