Quinolinic acid and glutamatergic neurodegeneration in Caenorhabditis elegans
Open accessAbstract
Quinolinic acid (QUIN) is an endogenous neurotoxin that acts as an N-methyl-D-aspartate receptor (NMDAR) agonist generating a toxic cascade, which can lead to neurodegeneration. The action of QUIN in Caenorhabditis elegans and the neurotoxins that allow the study of glutamatergic system disorders have not been carefully addressed. The effects of QUIN on toxicological and behavioral parameters in VM487 and VC2623 transgenic, as well as wild-type (WT) animals were performed to evaluate whether QUIN could be used as a neurotoxin in C. elegans. QUIN reduced survival of WT worms in a dose-dependent manner. A sublethal dose of QUIN (20 mM) increased reactive oxygen species (ROS) levels in an nmr-1/NMDAR-dependent manner, activated the DAF-16/FOXO transcription factor, and increased expression of the antioxidant enzymes, superoxide dismutase-3, glutathione S-transferase-4, and heat shock protein-16.2. QUIN did not change motor behavioral parameters, but altered the sensory behavior in N2 and VM487 worms. Notably, the effect of QUIN on the sensory behavioral parameters might occur, at least in part, secondary to increased ROS. However, the touch response behavior indicates a mechanism of action that is independent of ROS generation. In addition, non-lethal doses of QUIN triggered neurodegeneration in glutamatergic neurons. Our findings indicate that C. elegans might be useful as a model for studies of QUIN as a glutamatergic neurotoxin in rodent models.
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QUIN has neurotoxic effects, and at high concentrations, overstimulates the NMDA receptor resulting in glutamatergic excitotoxicity.
“QUIN has neurotoxic effects, and at high concentrations, overstimulates the NMDA receptor resulting in glutamatergic excitotoxicity (131).”
From Chronic stress, neuroinflammation, and depression: an overview of pathophysiological mechanisms and emerging anti-inflammatories (2023) · cites this paper as [131]
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- Authors
- da Silveira, T. L., Zamberlan, D. C., Arantes, L. P., Machado, M. L., da Silva, T. C., Câmara, D. D. F., Santamaría, A., Aschner, M., & Soares, F. A. A.
- Affiliations
- Universidade Federal de Santa Maria (BR)
- Albert Einstein College of Medicine (US)
- Venue
- NeuroToxicology
- Publisher
- Elsevier BV
- Published
- 2018-07
- Volume
- 67
- Pages
- 94-101
- ISSN
- 0161-813X (ISSN-L)
- PMC
- PMC6054819
- OpenAlex
- W2802016242
- Cited by
- 30
- References
- 54
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 6 · 2023: 4 · 2022: 6 · 2021: 2 · 2020: 5 · 2019: 1
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- NeuroToxicology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Programa de Apoio a Núcleos Emergentes (16/2551-0000248-7)
- NIEHS (R01 ES10563, 1R03 ES024849, ES07331, R21 ES025415)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Keywords
- quinolinic acid, NMDA receptor agonist, neurotoxins, reactive oxygen species, DAF-16/FOXO, antioxidant enzymes, sensory behavior, touch response, Caenorhabditis elegans, neurodegeneration model
- MeSH terms
- Animals, Dose-Response Relationship, Drug, Locomotion, Touch, Caenorhabditis elegans, Quinolinic Acid, Reactive Oxygen Species, Glutamic Acid, Neurodegenerative Diseases, Caenorhabditis elegans Proteins, Animals, Genetically Modified
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