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N-methyl d-aspartate receptor hypofunction reduces steady state visual evoked potentials.

Alexander Schielke, Bart Krekelberg

Journal of Neurophysiology July 14, 2025 DOI: 10.1152/jn.00296.2024 (opens in new tab)

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Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Nonhuman primates
Intervention Ketamine
Dose subanesthetic dose
Topics Ketamine
Keywords Nmda receptor hypofunction Schizophrenia research Psychiatric disorders Neuropsychiatric conditions Mental health Ssvep biomarkers Brain activity Brain rhythms Neural oscillations Evoked potentials Nmda receptor dysfunction Glutamatergic dysfunction Ketamine models Pharmacological models Nonhuman primate models Drug-induced models
Key findings NMDAR hypofunction induced by ketamine substantially reduced SSVEPs across 5 to 40 Hz, consistent with findings in schizophrenia.

Abstract

The dynamic coordination of neural activity across populations of neurons is impaired in neuropsychiatric disorders. Here, we focused on the large-scale rhythmic responses induced by flickering light. These so-called steady-state visual evoked potentials (SSVEPs) are reduced in people with schizophrenia (Sz). A large body of work has identified hypofunction of the N-methyl d-aspartate receptor (NMDAR) as a potential contributor to the symptoms of Sz. Here, we tested the hypothesis that NMDAR hypofunction can account for a reduced ability to generate the coordinated activity reflected in SSVEPs. We recorded SSVEPs using multielectrode arrays permanently implanted in the primary visual cortex of nonhuman primates. In separate sessions, animals were injected with saline (control) or a subanesthetic dose of ketamine (an NMDAR antagonist) to induce a NMDAR hypofunction state. SSVEPs generated during NMDAR hypofunction were substantially reduced and, consistent with findings in Sz, this reduction was found across a range of frequencies from 5 to 40 Hz. These findings provide novel insight into the role of NMDAR hypofunction in the generation of altered coordinated activity and provide experimental support for the hypothesis that NMDAR hypofunction underlies some of the symptoms of schizophrenia.

Comparable studies

Other preclinical and animal studies on ketamine, most cited first.

Study Year Design Participants
mTOR-Dependent Synapse Formation Underlies the Rapid Antidepressant Effects of NMDA Antagonists Rats 2010 Observational study
Activation of Glutamatergic Neurotransmission by Ketamine: A Novel Step in the Pathway from NMDA Receptor Blockade to Dopaminergic and Cognitive Disruptions Associated with the Prefrontal Cortex Conscious rats 1997 Dose-response study with microdialysis and behavioral testing
NMDAR inhibition-independent antidepressant actions of ketamine metabolites Mice 2016 Preclinical study
The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N‐methyl‐aspartate Spinal neurons in decerebrate or pentobarbitone-anaesthetized cats and rats 1983 Experimental study
R-ketamine: a rapid-onset and sustained antidepressant without psychotomimetic side effects Mice 2015 Experimental study

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