Alterations of Cortical GABA Neurons and Network Oscillations in Schizophrenia View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-08

AUTHORS

Guillermo Gonzalez-Burgos, Takanori Hashimoto, David A. Lewis

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. More... »

PAGES

335-344

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s11920-010-0124-8

    DOI

    http://dx.doi.org/10.1007/s11920-010-0124-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1050379284

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/20556669


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