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Curr Psychiatry Rep. 2010 Aug;12(4):335-44. doi: 10.1007/s11920-010-0124-8.

Alterations of cortical GABA neurons and network oscillations in schizophrenia.

Author information

1
Department of Psychiatry, Translational Neuroscience Program, University of Pittsburgh School of Medicine, Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15261, USA. gburgos@pitt.edu

Abstract

The hypothesis that alterations of cortical inhibitory gamma-aminobutyric acid (GABA) neurons are a central element in the pathology of schizophrenia has emerged from a series of postmortem studies. How such abnormalities may contribute to the clinical features of schizophrenia has been substantially informed by a convergence with basic neuroscience studies revealing complex details of GABA neuron function in the healthy brain. Importantly, activity of the parvalbumin-containing class of GABA neurons has been linked to the production of cortical network oscillations. Furthermore, growing knowledge supports the concept that gamma band oscillations (30-80 Hz) are an essential mechanism for cortical information transmission and processing. Herein we review recent studies further indicating that inhibition from parvalbumin-positive GABA neurons is necessary to produce gamma oscillations in cortical circuits; provide an update on postmortem studies documenting that deficits in the expression of glutamic acid decarboxylase67, which accounts for most GABA synthesis in the cortex, are widely observed in schizophrenia; and describe studies using novel, noninvasive approaches directly assessing potential relations between alterations in GABA, oscillations, and cognitive function in schizophrenia.

PMID:
20556669
PMCID:
PMC2919752
DOI:
10.1007/s11920-010-0124-8
[Indexed for MEDLINE]
Free PMC Article

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