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Related Concept Videos

Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

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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...
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Indirect-Acting Cholinergic Agonists: Pharmacokinetics01:22

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Indirect-acting cholinergic agonists, or anticholinesterases, enhance the body's cholinergic activity by inhibiting acetylcholine's breakdown. They are categorized as reversible or irreversible agents based on their mechanism of action. They are further classified into short-acting, intermediate-acting, and long-acting agents based on their duration of action.
Reversible agents containing quaternary amines, such as neostigmine and edrophonium, are not easily absorbed orally because they...
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Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

Indirect-Acting Cholinergic Agonists: Mechanism of Action

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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,...
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Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

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

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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...
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Toxic Reactions: Overview01:26

Toxic Reactions: Overview

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When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
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Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

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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...
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Expression of Concern "Acute exposure to sarin increases blood brain barrier permeability and induces neuropathological changes in the rat brain: Dose-response relationships" [Neurosci. 113(3) (2002) 721-741].

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Early differential cell death and survival mechanisms initiate and contribute to the development of OPIDN: a study of molecular, cellular, and anatomical parameters.

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Related Experiment Video

Updated: Feb 18, 2026

Electrophysiological Recording of The Central Nervous System Activity of Third-Instar Drosophila Melanogaster
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Organophosphorus ester-induced delayed neurotoxicity

M B Abou-Donia

    Annual Review of Pharmacology and Toxicology
    |January 1, 1981
    PubMed
    Summary

    Organophosphorus esters can cause delayed neurotoxicity (OPIDN) in humans and animals, leading to ataxia and paralysis. The exact mechanism remains unknown, but it involves protein phosphorylation in the nervous system.

    Area of Science:

    • Toxicology
    • Neuroscience
    • Environmental Health

    Background:

    • Organophosphorus esters (OPEs) are widely used pesticides.
    • Exposure to certain OPEs can induce Organophosphorus Ester-Induced Delayed Neurotoxicity (OPIDN).
    • OPIDN is characterized by a latent period followed by ataxia and paralysis, with axonal and myelin degeneration.

    Purpose of the Study:

    • To provide an up-to-date overview of OPIDN.
    • To highlight the significance of understanding the neurotoxic action of OPEs.
    • To discuss potential mechanisms and structure-activity relationships.

    Main Methods:

    • Review of existing literature on OPIDN.
    • Analysis of clinical manifestations and pathological findings.
    • Correlation of chemical structure with neurotoxic potency.

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    Oral Administration of Rotenone using a Gavage and Image Analysis of Alpha-synuclein Inclusions in the Enteric Nervous System
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    Oral Administration of Rotenone using a Gavage and Image Analysis of Alpha-synuclein Inclusions in the Enteric Nervous System
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    Main Results:

    • OPIDN affects both peripheral and central nervous systems.
    • Recovery is limited in severe cases, often resulting in upper motor neuron lesions.
    • Structure-activity studies suggest hydrophobic regions near the neurotoxicity target protein's active site.

    Conclusions:

    • The precise mechanism of OPIDN is still not fully understood.
    • Phosphorylation of a neurotoxicity target protein is a proposed initial event.
    • Further research is needed to elucidate OPIDN mechanisms and inform pesticide safety regulations.