The International Journal of Neuropsychopharmacology



Review Article

The GABAergic system in schizophrenia


Brian Paul  Blum  a1 c1 and J. John  Mann  a1
a1 Columbia University College of Physicians and Surgeons, Department of Psychiatry New York State Psychiatric Institute, Department of Neuroscience, New York, USA

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.

(Received July 18 2001)
(Reviewed November 11 2001)
(Revised January 28 2002)
(Accepted January 30 2002)


Key Words: CSF; GABA; post-mortem; schizophrenia.

Correspondence:
c1 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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