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...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

Indirect-Acting Cholinergic Agonists: Pharmacological Actions

Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
Drug Toxicity: Overview01:00

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
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,...
Drug Toxicity: Risk factors01:24

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...

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
Same journal

Nephronophthisis: Current clinical spectrum and molecular pathogenesis.

The FEBS journal·2026
Same journal

PDC1 deficiency results in 2-deoxyglucose sensitivity through inhibition of Pdc2 activity in yeast.

The FEBS journal·2026
Same journal

Epigenetic regulation of the hepcidin gene expression in hepatoma cells.

The FEBS journal·2026
Same journal

Loss of Ambp ameliorates steatosis progression by activating PPARα signaling in zebrafish.

The FEBS journal·2026
Same journal

Varying susceptibility of subpopulations along the epithelial-mesenchymal spectrum to undergo EMT.

The FEBS journal·2026
Same journal

ALOX15 links lipid metabolism to receptor trafficking in platelet activation.

The FEBS journal·2026
See all related articles

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: neurotoxicity.

Gilles J Guillemin1

  • 1Department of Pharmacology, University of New South Wales, Sydney, Australia.

The FEBS Journal
|January 19, 2012
PubMed
Summary
This summary is machine-generated.

Quinolinic acid causes cellular toxicity, impacting diseases like HIV-associated neurocognitive disorders, depression, and schizophrenia. This review covers therapeutic strategies targeting its production and effects.

More Related Videos

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

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

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity
07:42

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Published on: April 26, 2012

Area of Science:

  • Neuroscience
  • Toxicology
  • Pharmacology

Background:

  • Quinolinic acid (QA) is an endogenous NMDA receptor agonist with neurotoxic properties.
  • Elevated QA levels are implicated in various neurological and psychiatric disorders.

Discussion:

  • This review examines the cellular toxicity mechanisms of QA.
  • It explores QA's role in the pathogenesis of HIV-associated neurocognitive disorders (HAND), depressive disorders, and schizophrenia.

Key Insights:

  • QA contributes to neuronal damage and dysfunction in specific disease contexts.
  • Understanding QA's molecular pathways is crucial for disease management.

Outlook:

  • Future research should focus on developing novel therapeutic agents targeting QA.
  • Interfering with QA production or its downstream effects offers potential treatment strategies.