Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
Antidotes01:17

Antidotes

Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

Indirect-acting cholinergic agonists are agents that interact with the acetylcholinesterase enzyme in the synaptic cleft, preventing the breakdown of acetylcholine into choline and acetate. Consequently, the concentration of acetylcholine in the synaptic cleft increases. These agonists can be classified into reversible and irreversible inhibitors based on their duration of action.
Reversible inhibitors display short to medium durations of action. Short-acting agents include simple alcohols with...
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

Indirect-Acting Cholinergic Agonists: Mechanism of Action

Indirect-acting cholinergic agonists work by interacting with an enzyme called acetylcholinesterase (AChE) in the synaptic cleft. They can be reversible or irreversible inhibitors and have different effects on the enzyme.
Reversible inhibitors like edrophonium bind to a specific part of the enzyme called the anionic catalytic site. They form noncovalent bonds, which means they are not strongly attached to the enzyme. This creates a temporary and less stable enzyme–inhibitor complex, leading to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Retraction Note: Mapping NAD<sup>+</sup> metabolism in the brain of ageing Wistar rats: potential targets for influencing brain senescence.

Biogerontology·2026
Same author

Mapping the complexity of ME/CFS: Evidence for abnormal energy metabolism, altered immune profile, and vascular dysfunction.

Cell reports. Medicine·2025
Same author

Plasma soluble TREM2 is associated with plasma pTau-181 and pTau-231 in cognitively normal older adults at risk of Alzheimer's disease.

Journal of Alzheimer's disease : JAD·2025
Same author

Retraction: Consumption of pomegranates improves synaptic function in a transgenic mice model of Alzheimer's disease.

Oncotarget·2025
Same author

Retraction Note: Asiatic Acid Attenuated Aluminum Chloride-Induced Tau Pathology, Oxidative Stress and Apoptosis Via AKT/GSK-3β Signaling Pathway in Wistar Rats.

Neurotoxicity research·2025
Same author

Retraction Note: Naringenin Decreases α-Synuclein Expression and Neuroinflammation in MPTP-Induced Parkinson's Disease Model in Mice.

Neurotoxicity research·2025

Related Experiment Video

Updated: May 25, 2026

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry
10:58

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry

Published on: September 27, 2020

Quinolinic acid, the inescapable neurotoxin.

Gilles J Guillemin1

  • 1Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia. g.guillemin@unsw.edu.au

The FEBS Journal
|January 18, 2012
PubMed
Summary

Quinolinic acid (QUIN), a neurotoxin, plays a significant role in neuroinflammation by activating N-methyl-D-aspartate receptors and damaging brain cells. Recent findings highlight its multifaceted cytotoxic effects and impact on the blood-brain barrier.

More Related Videos

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
10:30

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators

Published on: December 27, 2013

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
14:10

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors

Published on: November 14, 2014

Related Experiment Videos

Last Updated: May 25, 2026

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry
10:58

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry

Published on: September 27, 2020

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
10:30

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators

Published on: December 27, 2013

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
14:10

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors

Published on: November 14, 2014

Area of Science:

  • Neuroscience
  • Immunology
  • Toxicology

Background:

  • Quinolinic acid (QUIN) involvement in neuroinflammation has grown significantly over the past two decades.
  • QUIN is produced by macrophages and microglia in the brain during neuroinflammatory conditions.
  • QUIN acts as an N-methyl-D-aspartate receptor agonist, functioning as an endogenous excitotoxin.

Purpose of the Study:

  • To review recent findings on the effects of quinolinic acid (QUIN).
  • To elucidate the various modes of action through which QUIN exerts its effects.
  • To consolidate current knowledge on QUIN's role in neuroinflammation and neurotoxicity.

Main Methods:

  • Literature review of recent scientific findings.
  • Analysis of studies investigating QUIN's mechanisms of action.
  • Synthesis of data on QUIN's cytotoxic and proinflammatory properties.

Main Results:

  • QUIN exhibits multiple cytotoxic mechanisms beyond excitotoxicity.
  • QUIN functions as a neurotoxin, gliotoxin, and proinflammatory mediator.
  • QUIN can act as a pro-oxidant and compromise blood-brain barrier integrity.

Conclusions:

  • QUIN is a key molecule in neuroinflammatory processes with diverse detrimental effects.
  • Understanding QUIN's mechanisms is crucial for developing therapeutic strategies for neuroinflammatory diseases.
  • Further research is needed to fully comprehend and counteract QUIN's neurotoxic actions.