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Related Concept Videos

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...
Direct-Acting Cholinergic Agonists: Pharmacokinetics01:31

Direct-Acting Cholinergic Agonists: Pharmacokinetics

Direct-acting cholinergic agonists, such as synthetic choline esters and naturally occurring alkaloids, exert their effects by enhancing the actions of acetylcholine and stimulating the parasympathetic nervous system. Synthetic choline esters share structural similarities with acetylcholine. For example, they have a positively charged quaternary ammonium or onium group, contributing to their hydrophilic characteristics. As a result, they are poorly absorbed in the body through oral...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
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...

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Related Experiment Video

Updated: Jun 19, 2026

Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test
08:06

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Published on: January 15, 2010

Drastic decrease in dopamine receptor levels in the striatum of acetylcholinesterase knock-out mouse.

Anna Hrabovska1, Vladimir Farar, Veronique Bernard

  • 1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, Bratislava, Slovakia. anna.hrabovska@gmail.com

Chemico-Biological Interactions
|October 13, 2009
PubMed
Summary

Acetylcholinesterase knock-out mice survive lethal acetylcholine levels due to adaptations in neuronal systems. Dopaminergic systems show significant receptor down-regulation, maintaining cellular homeostasis.

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Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease
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Published on: February 2, 2021

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Acetylcholinesterase knock-out mice survive high brain acetylcholine concentrations lethal to wild-type animals.
  • Survival involves reduced muscarinic, nicotinic, and adrenoceptor levels.

Purpose of the Study:

  • To investigate if the dopaminergic neuronal system also adapts in acetylcholinesterase knock-out mice.
  • To understand the compensatory mechanisms contributing to survival.

Main Methods:

  • Radioligand binding assays to measure dopamine receptor levels and binding affinity.
  • Immunohistochemistry to visualize dopamine transporter levels.
  • Measurement of intracellular cAMP and PI-phospholipase C activity.

Main Results:

  • Dopamine D(1)-like receptors decreased 28-fold and D(2)-like receptors decreased 37-fold, with normal binding affinity.
  • Dopamine transporter levels remained unaffected.
  • Intracellular cAMP and PI-phospholipase C activity were normal.

Conclusions:

  • Survival is linked to adaptations in cholinergic, adrenergic, and dopaminergic systems.
  • These adaptations balance cholinergic overstimulation and maintain cellular homeostasis.
  • The dopaminergic system adapts through significant receptor down-regulation.