Baseline Gamma Power during Auditory Steady-State Stimulation in Schizophrenia

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Baseline Gamma Power during Auditory Steady-State Stimulation in Schizophrenia

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Title: Baseline Gamma Power during Auditory Steady-State Stimulation in Schizophrenia
Author: Spencer, Kevin M.
Citation: Spencer, Kevin M. 2012. Baseline gamma power during auditory steady-state stimulation in schizophrenia. Frontiers in Human Neuroscience 5:190.
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Abstract: Several studies have reported deficits in \(\gamma\) oscillatory activity elicited by sensory stimulation or cognitive processes in schizophrenia patients (SZ) compared to healthy control subjects (HC). However, the evidence for cortical hyperexcitability and reduced function of N-methyl-D-aspartate receptors (NMDARs) on parvalbumin-expressing inhibitory interneurons in schizophrenia leads to the prediction that \(\gamma\) activity should rather be increased in SZ, but data supporting this hypothesis have been lacking. One possibility is that baseline induced \(\gamma\) power is increased, an effect that might have gone unnoticed in studies of stimulus-locked oscillations. Here we addressed this question by re-analyzing the data from a previously published study on the 40 Hz auditory steady-state response (ASSR) in schizophrenia in which dipole source localization was used to examine \(\gamma\) responses in the left and right auditory cortices. Subjects were 16 HC and 18 chronic SZ, who listened to trains of clicks presented at 40 Hz during electroencephalogram recording. Independent component analysis was used to remove ocular artifacts. Power spectra were computed for the pre-stimulus baseline period. We found that baseline power was higher in SZ than HC at 40 Hz in the left auditory cortex. Baseline 40 Hz power in the left auditory cortex was also correlated with ASSR evoked power in SZ. Thus, \(\gamma\) oscillation abnormalities in schizophrenia may include abnormal increases in baseline power as well as deficits in evoked oscillations. These baseline increases could be the sign of NMDAR hypofunction on parvalbumin-expressing inhibitory interneurons, which would be consistent with acute NMDAR antagonism and genetic ablation models of schizophrenia.
Published Version: doi:10.3389/fnhum.2011.00190
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