Visually induced MEG gamma-band oscillations in a human pharmacological model of psychosis D Rivolta1, A Sauer1, T Heidegger2, K Birkner1, B Scheller2, M Wibral3, W Singer4, P J Uhlhaas5 |
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1Department of Neurophysiology, Max Planck Institute for Brain Research, Germany |
| Aberrant neural oscillations in the gamma-band range (>30 Hz) are crucially involved in the pathophysiology of schizophrenia. Dysfunctional gamma-band-activity can be driven by disrupted glutamatergic neurotransmission mediated by the N-methyl-D-aspartate (NMDA) receptor. In this study, we examined the effects of NMDA-receptor hypofunctioning on gamma-band-activity during the administration of ketamine in human participants. Neural oscillations induced by sinusoidal gratings were recorded using Magnetoencephalography (MEG) in a group of 15 healthy volunteers. We also recorded resting state activity. Each participant received an intravenous injection of a sub-anesthetic dose of ketamine and a placebo saline solution in a within-subject design. Results show that ketamine, compared to placebo, led to an increase of visually-induced gamma band oscillations (45-75 Hz) over occipital sensors, with sources localized to early visual areas. Ketamine also increased gamma-activity (30-60 Hz) at rest over fronto-central sensors, with sources localized in the right anterior cingulum and left orbito-frontal cortex. The ketamine-induced gamma-band-activity upregulation can be explained by the shift in the excitation/inhibition balance in favor of excitation of pyramidal cells due to hypofunctioning NMDA-receptor. Since the upregulation of gamma-band activity has been described in early psychosis, our results support the clinical relevance of the NMDA-receptor hypofunctioning model of schizophrenia. |
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