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Gamma Oscillations and Excitation/Inhibition Imbalance: Parallel Effects of NMDA Receptor Antagonism and Psychosis.

Brian J Roach, Judith M. Ford, Spero Nicholas, Jamie M Ferri, Handan Gunduz-Bruce, John H. Krystal, Judith Jaeger, Daniel H. Mathalon

Biological psychiatry. Cognitive neuroscience and neuroimaging January 18, 2025 DOI: 10.1016/j.bpsc.2025.01.008 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Crossover, placebo-controlled drug challenge study and case-control study Peer reviewed
Population Healthy participants and patients with schizophrenia
Intervention Ketamine
Topics Ketamine
Keywords Electroencephalography EEG Nmda receptor nmdar Schizophrenia Mental illness research Gamma waves Assr EEG Patterns
Citations 7
Key findings Ketamine-induced 40-Hz ASSR abnormalities resembled those in schizophrenia except for phase, supporting NMDA receptor hypofunction's role in gamma oscillation deficits in schizophrenia.

Abstract

Auditory steady-state response (ASSR) abnormalities in the 40-Hz (gamma band) frequency have been observed in schizophrenia and in rodent studies of NMDA receptor (NMDAR) hypofunction. However, the extent to which 40-Hz ASSR abnormalities in schizophrenia resemble deficits in 40-Hz ASSR induced by acute administration of ketamine, an NMDAR antagonist, is not yet known. To address this knowledge gap, we conducted parallel electroencephalography studies: a crossover, placebo-controlled ketamine drug challenge study with healthy participants (study 1) and a comparison of patients with schizophrenia and healthy control participants (study 2). Time-frequency analysis of the ASSR was used to calculate baseline, broadband gamma power, evoked power, total power, phase-locking factor, and phase-locking angle. Relative to healthy control participants, patients with schizophrenia exhibited increases in prestimulus broadband gamma power and reductions in 40-Hz ASSR evoked power, total power, and phase-locking factor, replicating previous studies. However, we failed to replicate previous findings of 40-Hz ASSR phase delay in schizophrenia. Relative to placebo, ketamine increased prestimulus broadband gamma power; reduced 40-Hz ASSR evoked power, total power, and phase-locking factor; and advanced the phase of the 40-Hz ASSR. Normalized by their respective control groups/conditions, direct comparison of these measures between schizophrenia and ketamine data only revealed significant differences in phase, supporting the role of NMDAR hypofunction in mediating gamma oscillation abnormalities in schizophrenia.

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