Cited by 241Tryptophan and brain disordersSchizophrenia research and treatmentTreatment of Major Depression

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Interleukin-6 Mediates the Increase in NADPH-Oxidase in the Ketamine Model of Schizophrenia

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Behrens, M. Margarita, Ali, Sameh S., Dugan, Laura L.·2008·The Journal of Neuroscience

DOI 10.1523/jneurosci.4457-08.2008PMC PMC2752712

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Abstract

Adult exposure to NMDA receptor antagonists, such as ketamine, produces psychosis in humans, and exacerbates symptoms in schizophrenic patients. We recently showed that ketamine activates the innate immune enzyme NADPH-oxidase in brain, and that the superoxide produced leads to dysfunction of a subset of fast-spiking inhibitory interneurons expressing the calcium-binding protein parvalbumin (PV). Here we show that neuronal production of interleukin-6 (IL-6) is necessary and sufficient for ketamine-mediated activation of NADPH-oxidase in brain. Removal of IL-6 in neuronal cultures by anti-IL-6 blocking antibodies, or in vivo by use of IL-6-deficient mice, prevented the increase in superoxide by ketamine and rescued the interneurons. Accumulating evidence suggests that schizophrenia patients suffer from diminished antioxidant defenses, and a recent clinical trial showed that enhancing these defenses may ameliorate symptoms of the disease. Our results showing that ketamine-induced IL-6 is responsible for the activation of NADPH-oxidase in brain suggest that reducing brain levels of this cytokine may protect the GABAergic phenotype of fast-spiking PV-interneurons and thus attenuate the propsychotic effects of ketamine.

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Authors: Behrens, M. M., Ali, S. S., & Dugan, L. L.
Affiliations: University of California San Diego (US)
ORCID: Behrens, M. Margarita
Ali, Sameh S.
Dugan, Laura L.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2008-12-17
Volume: 28
Issue: 51
Pages: 13957-13966
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.4457-08.2008
PMC: PMC2752712
OpenAlex: W2062030838
Cited by: 241
References: 52
Citations by year: 2026: 5 · 2025: 7 · 2024: 7 · 2023: 9 · 2022: 11 · 2021: 9 · 2020: 14 · 2019: 8 · 2018: 13 · 2017: 13 · 2016: 18 · 2015: 20 · 2014: 23 · 2013: 17 · 2012: 28
FWCI: 4.37
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 182 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Hartford Foundation for Public Giving
Larry L. Hillblom Foundation
National Institute on Aging (K25AG026379, R21AG030320)
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
Keywords: interleukin-6, NADPH oxidase, ketamine, schizophrenia, NMDA receptor antagonists, superoxide, parvalbumin interneurons, fast-spiking interneurons, GABAergic interneurons, antioxidant defense, cytokine inhibition, IL-6-deficient mice
MeSH terms: Animals, Antibodies, Cells, Cultured, Disease Models, Animal, Enzyme Activation, gamma-Aminobutyric Acid, Interneurons, Ketamine, Male, Mice, Inbred C57BL, RNA, Messenger, Schizophrenia, Superoxides, Interleukin-6, Prefrontal Cortex, Mice, Knockout, NADPH Oxidases, Mice

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Interleukin-6 Mediates the Increase in NADPH-Oxidase in the Ketamine Model of Schizophrenia

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