ArticleNPJ schizophrenia2017
Vulnerability to omega-3 deprivation in a mouse model of NMDA receptor hypofunction.
Article in NPJ schizophrenia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Polyunsaturated fatty acids and psychotic disorders: integrating mechanistic, genetic, and clinical evidence.Frontiers in nutrition · 2026Review
- Combination of Haloperidol With UNC9994, β-arrestin-Biased Analog of Aripiprazole, Ameliorates Schizophrenia-Related Phenotypes Induced by NMDAR Deficit in Mice.The international journal of neuropsychopharmacology · 2024Article
- Abnormal sensory perception masks behavioral performance of Grin1 knockdown mice.Genes, brain, and behavior · 2022Article
- Consequences of NMDA receptor deficiency can be rescued in the adult brain.Molecular psychiatry · 2021Article
- Shared Biological Pathways between Antipsychotics and Omega-3 Fatty Acids: A Key Feature for Schizophrenia Preventive Treatment?International journal of molecular sciences · 2021Review
- A novel allosteric modulator of the cannabinoid CBNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Discordant Dose-Dependent Metabolic Effects of Eicosapentanoic Acid in Diet-Induced Obese Mice.Nutrients · 2020Article
- Remembering Mechanosensitivity of NMDA Receptors.Frontiers in cellular neuroscience · 2019Review
- The use of antioxidant compounds in the treatment of first psychotic episode: Highlights from preclinical studies.CNS neuroscience & therapeutics · 2018Review
- N-3 (Omega-3) Fatty Acids: Effects on Brain Dopamine Systems and Potential Role in the Etiology and Treatment of Neuropsychiatric Disorders.CNS & neurological disorders drug targets · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have found decreased levels of ω-3 polyunsaturated fatty acids in the brain and blood of schizophrenia patients. Furthermore, dietary ω-3 supplements may improve schizophrenia symptoms and delay the onset of first-episode psychosis. We used an animal model of NMDA receptor hypofunction, NR1KD mice, to understand whether changes in glutamate neurotransmission could lead to changes in brain and serum fatty acids. We further asked whether dietary manipulations of ω-3, either depletion or supplementation, would affect schizophrenia-relevant behaviors of NR1KD mice. We discovered that NR1KD mice have elevated brain levels of ω-6 fatty acids regardless of their diet. While ω-3 supplementation did not improve any of the NR1KD behavioral abnormalities, ω-3 depletion exacerbated their deficits in executive function. Omega-3 depletion also caused extreme mortality among male mutant mice, with 75% mortality rate by 12 weeks of age. Our studies show that alterations in NMDAR function alter serum and brain lipid composition and make the brain more vulnerable to dietary ω-3 deprivation.
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Registered trials
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