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Suppression of γ-Oscillations in the Dorsolateral Prefrontal Cortex following Long Interval Cortical Inhibition: A TMS–EEG Study.

Authors :
Farzan, Faranak
Barr, Mera S.
Wong, Willy
Chen, Robert
Fitzgerald, Paul B.
Daskalakis, Zafiris J.
Source :
Neuropsychopharmacology. May2009, Vol. 34 Issue 6, p1543-1551. 9p. 1 Color Photograph, 4 Graphs.
Publication Year :
2009

Abstract

Gamma (γ)-oscillations (30–50 Hz) represent important electrophysiological measures, which are generated through the execution of higher order cognitive tasks (eg, working memory) in the dorsolateral prefrontal cortex (DLPFC). By contrast, cortical inhibition (CI) refers to a neurophysiological process in which GABAergic inhibitory interneurons selectively suppress the activation of other neurons in the cortex. Recently, abnormalities in both CI and γ-oscillations have been associated with various neuropsychiatric disorders including schizophrenia. Animal research suggests that suppression of γ-oscillations is, in part, mediated through GABAergic inhibitory neurotransmission. However, no such evidence has been demonstrated in human, largely because of technological limitations. Recently, we reported on novel methods permitting the recording of CI from the DLPFC through transcranial magnetic stimulation (TMS) combined with electroencephalography (EEG). The aim of this study was to examine the effects of GABAergic inhibitory neurotransmission on γ-oscillations by combining TMS with EEG. Long interval cortical inhibition (LICI), a paired TMS paradigm, was used to index GABAB receptor mediated inhibitory neurotransmission in the motor cortex and DLPFC of healthy individuals. γ-Oscillations were significantly inhibited by LICI (38.1±26.5%; p0.013) in the DLPFC but not in the motor cortex. These results provide neurophysiological evidence to demonstrate γ-oscillations are inhibited by LICI in the DLPFC but not in the motor cortex. Such specificity suggests that the modulation of γ-oscillations may represent an important neurophysiological process that may, in part, be responsible for optimal DLPFC functioning in healthy human subjects.Neuropsychopharmacology (2009) 34, 1543–1551; doi:10.1038/npp.2008.211; published online 26 November 2008 [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
0893133X
Volume :
34
Issue :
6
Database :
Academic Search Index
Journal :
Neuropsychopharmacology
Publication Type :
Academic Journal
Accession number :
37591389
Full Text :
https://doi.org/10.1038/npp.2008.211