Abstract
Several studies have reported deficits in γ 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 γ activity should rather be increased in SZ, but data supporting this hypothesis have been lacking. One possibility is that baseline induced γ 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 γ 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, γ 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.
Highlights
Oscillatory activity in the γ band (30–100 Hz) of the electroencephalogram (EEG) has been proposed to be sensitive to cortical circuit abnormalities in schizophrenia (e.g., Kwon et al, 1999; Spencer et al, 2003; Lewis et al, 2005)
For the right hemisphere (RH) tangential dipole, baseline power appeared to be slightly increased in schizophrenia patients (SZ) compared to healthy control subjects (HC) from 36 to 72 Hz (Figure 2B), but this effect was not significant [t(32) = 0.669, p = 0.509], nor did 40 Hz baseline power differ between groups [t(32) = 0.502, p = 0.619]
Given the evidence suggesting that increased baseline activity may be related to psychotic symptoms, hallucinations, we examined correlations between left hemisphere (LH) radial dipole baseline 40 Hz power and psychotic symptom scales (Total Positive Symptoms, Global Rating of Hallucinations, and Auditory Hallucinations) of the Scale for the Assessment of Positive Symptoms (SAPS)
Summary
Oscillatory activity in the γ band (30–100 Hz) of the electroencephalogram (EEG) has been proposed to be sensitive to cortical circuit abnormalities in schizophrenia (e.g., Kwon et al, 1999; Spencer et al, 2003; Lewis et al, 2005). One of the neurophysiological consequences of acute NMDAR administration in humans and animals is increased cortical excitability (e.g., Di Lazzaro et al, 2003; Homayoun and Moghaddam, 2007), which has led to the hypothesis that NMDAR antagonists produce their schizophrenia-like effects primarily by reducing the excitation of inhibitory interneurons, leading to a disinhibition of pyramidal cells and increased excitability (Olney et al, 1991; Moghaddam et al, 1997). Heckers et al (1998) observed increased baseline activity in the hippocampus in SZ
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