ArticleNeurotoxicology2018
Quinolinic acid and glutamatergic neurodegeneration in Caenorhabditis elegans.
Article in Neurotoxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Blood Metabolomic Profiling of Systemic Responses to Dried Black Lychee in a Scopolamine-Induced Cognitive Impairment in Rats.Biology · 2026Article
- Dimethyl fumarate ameliorates quinolinic acid-induced ageing and neurodegeneration in Caenorhabditis elegans.Biogerontology · 2026Article
- A Hypothesis: Metabolic Contributions to 16p11.2 Deletion Syndrome.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Article
- Amyloid β induces hormetic-like effects through major stress pathways in a C. elegans model of Alzheimer's Disease.PloS one · 2025Article
- Bee Venom Toxic Effect on MDA-MB-231 Breast Cancer Cells andAnti-cancer agents in medicinal chemistry · 2024Article
- Alzheimer's disease and its treatment-yesterday, today, and tomorrow.Frontiers in pharmacology · 2024Review
- Butyrate ameliorates quinolinic acid-induced cognitive decline in obesity models.The Journal of clinical investigation · 2023Article
- Chronic stress, neuroinflammation, and depression: an overview of pathophysiological mechanisms and emerging anti-inflammatories.Frontiers in psychiatry · 2023Review
- Quinolinic Acid Induces Alterations in Neuronal Subcellular Compartments, Blocks Autophagy Flux and Activates Necroptosis and Apoptosis in Rat Striatum.Molecular neurobiology · 2022Article
- Caenorhabditis elegans as a model for studies on quinolinic acid-induced NMDAR-dependent glutamatergic disorders.Brain research bulletin · 2021Article
- Kynurenine Pathway of Tryptophan Metabolism in Neuropsychiatric Disorders: Pathophysiologic and Therapeutic Considerations.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2020Review
- Modeling neurodegeneration inDisease models & mechanisms · 2020Review
- Molecular Mechanisms of Glial Cells Related Signaling Pathways Involved in the Neuroinflammatory Response of Depression.Mediators of inflammation · 2020Review
- Effects of Sleep Deprivation on the Tryptophan Metabolism.International journal of tryptophan research : IJTR · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
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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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.