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The glutamatergic dysfunction hypothesis for schizophrenia

J T Coyle1

  • 1Consolidated Department of Psychiatry, Harvard Medical School, Boston, Mass., USA.

Harvard Review of Psychiatry
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

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Glutamate system dysfunction, particularly involving N-methyl-D-aspartate (NMDA) receptors, is implicated in schizophrenia. Enhancing NMDA receptor function may alleviate negative symptoms and cognitive deficits in patients.

Area of Science:

  • Neuroscience
  • Psychiatry

Background:

  • Schizophrenia is a complex syndrome with varied symptoms and etiologies.
  • Glutamatergic neurotransmission is crucial for excitatory signaling in the brain.

Purpose of the Study:

  • To review evidence linking corticolimbic glutamatergic dysfunction to schizophrenia.
  • To explore the role of N-methyl-D-aspartate (NMDA) receptors in schizophrenia.

Main Methods:

  • Review of existing scientific literature on glutamatergic systems and schizophrenia.
  • Examination of the effects of NMDA receptor antagonists and agonists.

Main Results:

  • NMDA receptor dysfunction is associated with schizophrenia symptoms.
  • Endogenous NMDA receptor antagonists may be elevated in schizophrenia patients.

Related Experiment Videos

  • NMDA receptor enhancing drugs show promise in treating negative symptoms and cognitive deficits.

    • Conclusions:

    • Glutamatergic neurotransmission dysfunction is a significant factor in schizophrenia.
    • Targeting NMDA receptors offers a potential therapeutic avenue for schizophrenia treatment.