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Schizophrenia Bulletin Advance Access published online on June 9, 2008
Schizophrenia Bulletin, doi:10.1093/schbul/sbn059
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© The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Region-Specific Changes in Gamma and Beta2 Rhythms in NMDA Receptor Dysfunction Models of Schizophrenia

Anita K. Roopun2, Mark O. Cunningham2, Claudia Racca2, Kai Alter2, Roger D. Traub3 and Miles A. Whittington1,2
2 Institute of Neuroscience, The Medical School, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK
3 Department of Physiology and Pharmacology, SUNY Downstate Medical Center, Brooklyn, NY 11203

1To whom correspondence should be addressed; tel: +44-191-222-5340, fax: +44 191 222 6992, e-mail: m.a.whittington{at}ncl.ac.uk.

Cognitive disruption in schizophrenia is associated with altered patterns of spatiotemporal interaction associated with multiple electroencephalogram (EEG) frequency bands in cortex. In particular, changes in the generation of gamma (30–80 Hz) and beta2 (20–29 Hz) rhythms correlate with observed deficits in communication between different cortical areas. Aspects of these changes can be reproduced in animal models, most notably those involving acute or chronic reduction in glutamatergic synaptic communication mediated by N-methyl D-aspartate (NMDA) receptors. In vitro electrophysiological and immunocytochemical approaches afforded by such animal models continue to reveal a great deal about the mechanisms underlying EEG rhythm generation and are beginning to uncover which basic molecular, cellular, and network phenomena may underlie their disruption in schizophrenia. Here we briefly review the evidence for changes in {gamma}-aminobutyric acidergic (GABAergic) and glutamatergic function and address the problem of region specificity of changes with quantitative comparisons of effects of ketamine on gamma and beta2 rhythms in vitro. We conclude, from available evidence, that many observed changes in markers for GABAergic function in schizophrenia may be secondary to deficits in NMDA receptor–mediated excitatory synaptic activity. Furthermore, the broad range of changes in cortical dynamics seen in schizophrenia—with contrasting effects seen in different brain regions and for different frequency bands—may be more directly attributable to underlying deficits in glutamatergic neuronal communication rather than GABAergic inhibition alone.

Keywords: schizophrenia / EEG / gamma / beta / inhibition / NMDA


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