The GABAergic system in schizophrenia
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.
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: [email protected]