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  • The International Journal of Neuropsychopharmacology, Volume 5, Issue 2
  • June 2002, pp. 159-179

The GABAergic system in schizophrenia

  • Brian Paul Blum (a1) and J. John Mann (a1)
  • DOI: http://dx.doi.org/10.1017/S1461145702002894
  • Published online: 01 July 2002
Abstract

A defect in neurotransmission involving γ-amino butyric acid (GABA) in schizophrenia was first proposed in the early 1970s. Since that time, a considerable effort has been made to find such a defect in components of the GABAergic system. After a brief introduction focusing on historical perspectives, this paper reviews post-mortem and other biological studies examining the following components of the GABAergic system in schizophrenic subjects: the GABA biosynthetic enzyme, glutamate decarboxylase; free GABA; the GABA transporter; the GABAA, GABAB and benzodiazepine receptors; and the catabolic enzyme GABA transaminase. Additionally, post-mortem studies using morphology or calcium-binding protein to identify GABAergic neurons are also reviewed. Substantial evidence argues for a defect in the GABAergic system of the frontal cortex in schizophrenia which is limited to the parvalbumin-class of GABAergic interneurons.

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Corresponding author
Address for correspondence: Dr B. P. Blum, New York State Psychiatric Institute, Department of Neuroscience, 1051 Riverside Drive, Unit 42, New York, NY, 10032, USA. Tel.: 212-543-6223 Fax: 212-543-6017 E-mail: bb453@columbia.edu
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The International Journal of Neuropsychopharmacology
  • ISSN: 1461-1457
  • EISSN: 1469-5111
  • URL: /core/journals/the-international-journal-of-neuropsychopharmacology
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