21. Contributions of Glutamate and GABA Systems to the Neurobiology and Treatment of Schizophrenia

  1. Daniel R. Weinberger MD4 and
  2. Paul J. Harrison MA, BM, BCh, DM(Oxon), FRCPsych5
  1. John H. Krystal MD1,2 and
  2. Bita Moghaddam PhD3

Published Online: 8 MAR 2011

DOI: 10.1002/9781444327298.ch21

Schizophrenia, Third Edition

Schizophrenia, Third Edition

How to Cite

Krystal, J. H. and Moghaddam, B. (2010) Contributions of Glutamate and GABA Systems to the Neurobiology and Treatment of Schizophrenia, in Schizophrenia, Third Edition (eds D. R. Weinberger and P. J. Harrison), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444327298.ch21

Editor Information

  1. 4

    Genes, Cognition and Psychosis Program, Clinical Studies Section, Clinical Brain Disorders Branch, National Institute of Health, Bethesda, MD, USA

  2. 5

    Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK

Author Information

  1. 1

    Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA

  2. 2

    Schizophrenia Biological Research Center (151 - D), VA Connecticut Healthcare System, West Haven, CT, USA

  3. 3

    Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA

Publication History

  1. Published Online: 8 MAR 2011
  2. Published Print: 10 DEC 2010

ISBN Information

Print ISBN: 9781405176972

Online ISBN: 9781444327298



  • contributions of glutamate and GABA systems - to neurobiology and treatment of schizophrenia;
  • glutamatergic and GABAergic neuropathology - in schizophrenia;
  • Glutamatergic neuropathology, in schizophrenia - and reduced glutamate neural connectivity;
  • NMDA receptors, stimulated - molecules of glutamate and glycine bind to a receptor, “activated” by membrane depolarization;
  • glutamate-related synaptic proteins - marked by a high degree of heterogeneity;
  • glutamate receptor subunit and synaptic proteins - in schizophrenia using postmortem brain samples;
  • metabotropic glutamate receptors (mGluR);
  • GABA receptors alterations in GABA receptor populations - heritable vulnerability to schizophrenia;
  • drugs, enhancing glutamatergic activation - cognitive deficits and reductions in cortical metabolism;
  • two approaches, reducing glutamate release - blocking voltage-gated cation channels and stimulating Group II mGlu receptors


This chapter contains sections titled:

  • Glutamatergic and GABAergic neuropathology in schizophrenia

  • Psychopharmacology and physiology of glutamate and GABA systems

  • Implications

  • Acknowledgements

  • References