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Updated: May 7, 2026
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Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry
Published on: September 27, 2020
Quinolinic acid: an endogenous neurotoxin with multiple targets.
Rafael Lugo-Huitrón1, Perla Ugalde Muñiz, Benjamin Pineda
1Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, S.S.A., 14269 México, DF, Mexico.
Oxidative Medicine and Cellular Longevity
|October 4, 2013
Summary
Quinolinic acid (QUIN), a neurotoxin, contributes to neurological diseases by overstimulating NMDA receptors. Its toxicity involves multiple mechanisms beyond NMDA receptor activation, impacting brain function and cell survival.
Area of Science:
- Neuroscience
- Neurochemistry
- Pathology
Background:
- Quinolinic acid (QUIN), a kynurenine pathway metabolite, is found in human brain and cerebrospinal fluid (CSF).
- Elevated QUIN levels are linked to the pathogenesis of various neurological diseases.
- QUIN acts as an N-methyl-D-aspartate (NMDA) receptor agonist with potent excitotoxic effects in vivo.
Purpose of the Study:
- To review the multifaceted neurotoxic targets of quinolinic acid.
- To explore mechanisms of QUIN neurotoxicity beyond NMDA receptor overactivation.
Main Methods:
- Literature review of studies on quinolinic acid neurotoxicity.
- Analysis of QUIN's interactions with neuronal targets and cellular processes.
Main Results:
- QUIN's excitotoxicity is partly mediated by NMDA receptor stimulation.
- Additional QUIN targets include presynaptic receptors, cellular energy metabolism, and oxidative stress pathways.
- QUIN affects transcription factors, cytoskeletal integrity, and behavior, ultimately leading to cell death.
Conclusions:
- QUIN neurotoxicity involves a complex interplay of multiple cellular targets.
- Understanding these diverse mechanisms is crucial for developing therapeutic strategies for QUIN-related neurological disorders.
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