ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
The Role of GluN2C-Containing NMDA Receptors in Ketamine's Psychotogenic Action and in Schizophrenia Models.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 69 citations in OpenAlex.
- Ketamine induces multiple individually distinct whole-brain functional connectivity signatures.eLife · 2024Trial
- GluN2D NMDA Receptors: Bridging Physiology and Pathology.Biological psychiatry · 2026Review
- The Role of the NMDA Receptor in the Treatment of Psychiatric and Neurological Diseases.Brain sciences · 2026Review
- Rapid antidepressant potential of nitrous oxide: current state and major questions.Molecular psychiatry · 2026Review
- Esketamine/Ketamine: Dual-Action Mechanisms and Clinical Prospects beyond Anesthesia in Psychiatry, Immunology, and Oncology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- GluN2D-containing NMDA receptors in parvalbumin neurons in the nucleus accumbens regulate nocifensive responses in neuropathic pain.Neurobiology of disease · 2025Article
- Contrasting patterns of extrasynaptic NMDAR-GluN2B expression in macaque subgenual cingulate and dorsolateral prefrontal cortices.Frontiers in neuroanatomy · 2025Article
- Ketamine can produce oscillatory dynamics by engaging mechanisms dependent on the kinetics of NMDA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Ketamine improves neuronal recovery following spreading depolarization in peri-infarct tissues.Journal of neurochemistry · 2024Article
- Ketamine can produce oscillatory dynamics by engaging mechanisms dependent on the kinetics of NMDA receptors.bioRxiv : the preprint server for biology · 2024Article
- Ketamine and the neurobiology of depression: Toward next-generation rapid-acting antidepressant treatments.Proceedings of the National Academy of Sciences of the United States of America · 2023Review
- The Role of Glutamate Underlying Treatment-resistant Depression.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023Review
- Distinct structure and gating mechanism in diverse NMDA receptors with GluN2C and GluN2D subunits.Nature structural & molecular biology · 2023Article
- Article
- Neuropsychiatric consequences of COVID-19 related olfactory dysfunction: could non-olfactory cortical-bound inputs from damaged olfactory bulb also contribute to cognitive impairment?Frontiers in neuroscience · 2023Article
- Structural insights into assembly and function of GluN1-2C, GluN1-2A-2C, and GluN1-2D NMDARs.Molecular cell · 2022Article
- Whole blood transcriptional signatures associated with rapid antidepressant response to ketamine in patients with treatment resistant depression.Translational psychiatry · 2022Article
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- The Sustained Antidepressant Effects of Ketamine Are Independent of the Lateral Habenula.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Symptomatologic pathomechanism ofEncephalitis (Seoul, Korea) · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The NMDA receptor (NMDAR) hypofunction hypothesis of schizophrenia is supported by multiple lines of evidence. Notably, administration of the NMDAR antagonist, ketamine, to healthy human subjects has psychotogenic action, producing both positive and negative symptoms associated with schizophrenia. NMDARs have multiple subtypes, but the subtypes through which ketamine produces its psychotogenic effects are not known. Here we address this question using quantitative data that characterize ketamine's ability to block different NMDAR subtypes. Our calculations indicate that, at a concentration that has psychotogenic action in humans, ketamine blocks a substantial fraction of GluN2C subunit-containing receptors but has less effect on GluN2A-, GluN2B-, and GluN2D-containing receptors. Thus, GluN2C-containing receptors may have preferential involvement in psychotic states produced by ketamine. A separate line of experiments also points to a special role for GluN2C. That work demonstrates the ability of NMDAR antagonists to mimic the elevation in the awake-state δ frequency EEG power that occurs in schizophrenia. Physiological experiments in rodents show that NMDAR antagonists generate δ oscillations by their action on the GluN2C-containing NMDARs that are prevalent in the thalamus. Optogenetic experiments suggest that such oscillations could contribute to symptoms of schizophrenia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.