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The glutamate hypothesis of schizophrenia: evidence from human brain tissue studies

  • Published:2014-10-14 Issue:1 Volume:1338 Page:38-57
  • ISSN:0077-8923
  • Container-title:Annals of the New York Academy of Sciences
  • language:en
  • Short-container-title:Ann. N.Y. Acad. Sci.

Author:

Hu Wei1,MacDonald Matthew L.2,Elswick Daniel E.1,Sweet Robert A.234

Affiliation:

1. Department of Behavioral Medicine and Psychiatry; West Virginia University Health Sciences Center; Morgantown West Virginia

2. Department of Psychiatry, University of Pittsburgh; Pittsburgh Pennsylvania

3. Department of Neurology, University of Pittsburgh; Pittsburgh Pennsylvania

4. VISN 4 Mental Illness Research; Education and Clinical Center (MIRECC); VA Pittsburgh Healthcare System; Pittsburgh Pennsylvania

Funder

National Institute of Mental Health

Publisher

Wiley

Subject

History and Philosophy of Science,General Biochemistry, Genetics and Molecular Biology,General Neuroscience

Reference181 articles.

1. Negative schizophrenic symptomatology and the PCP (phencyclidine) model of schizophrenia Hillside;Javitt;J. Clin. Psychiatry,1987

2. Recent advances in the phencyclidine model of schizophrenia;Javitt;Am. J. Psychiatry,1991

3. Glutamate receptor dysfunction and schizophrenia;Olney;Arch. Gen. Psychiatry,1995

4. The glutamatergic dysfunction hypothesis for schizophrenia;Coyle;Harv. Rev. Psychiatry,1996

5. Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses;Krystal;Arch. Gen. Psychiatry,1994

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