Frontal cortical and left temporal glutamatergic dysfunction in schizophrenia

J F Deakin, P Slater, D. M. Simpson, A C Gilchrist, W J Skan, M.C. Royston, Gavin P. Reynolds, A J Cross

Research output: Contribution to journalArticlepeer-review


Glutamatergic mechanisms have been investigated in postmortem brain samples from schizophrenics and controls. D-[3H]Aspartate binding to glutamate uptake sites was used as a marker for glutamatergic neurones, and [3H]kainate binding for a subclass of postsynaptic glutamate receptors. There were highly significant increases in the binding of both ligands to membranes from orbital frontal cortex on both the left and right sides of schizophrenic brains. The changes are unlikely to be due to antemortem neuroleptic drug treatment, because no similar changes were recorded in other areas. A predicted left-sided reduction in D-[3H]aspartate binding was refuted at 5% probability, but not at 10%. Previously reported high concentrations of dopamine in left amygdala were strongly associated with low concentrations of D-[3H]aspartate binding in left polar temporal cortex in the schizophrenics. The findings are compatible with an overabundant glutamatergic innervation of orbital frontal cortex in schizophrenia. The results also suggest that schizophrenia may involve left-sided abnormalities in the relationship between temporal glutamatergic and dopaminergic projections to amygdala.

Original languageEnglish
Pages (from-to)1781-1786
Number of pages6
JournalJournal of neurochemistry
Issue number6
Publication statusPublished - Jun 1989


  • Aspartic Acid
  • Dopamine
  • Frontal Lobe
  • Glutamates
  • Glutamic Acid
  • Humans
  • Schizophrenia
  • Temporal Lobe
  • Journal Article
  • Research Support, Non-U.S. Gov't


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