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Cholinergic neurotransmission involves the synthesis and the release of acetylcholine (ACh) in order to transmit nerve impulses across the synapse. The process begins with the synthesis of acetyl CoA, a precursor for ACh, from ATP, acetate, and coenzyme A in the mitochondria. Choline, another vital precursor, is transported inside the neuron through choline transporters, including high-affinity choline transporter CHT1, low-affinity choline transporter CTL1, and lower-affinity choline...
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The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
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Cholinergic Receptors: Nicotinic01:15

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Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
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Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

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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.
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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.
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Cholinergic agonists or cholinomimetics mimic the action of acetylcholine to stimulate the parasympathetic nervous system. They are categorized into direct-acting and indirect-acting agents. The direct-acting cholinergic drugs induce the parasympathetic response by directly binding to the muscarinic or nicotine receptors. In comparison, the indirect-acting cholinergic drugs prevent acetylcholine hydrolysis, indirectly contributing to the extended parasympathetic response.
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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
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Asynchronous subunit transitions prime acetylcholine receptor activation.

Mackenzie J Thompson1, Christian J G Tessier2, Anna Ananchenko1

  • 1Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada.

Science (New York, N.Y.)
|October 2, 2025
PubMed
Summary
This summary is machine-generated.

Agonist binding to muscle nicotinic acetylcholine receptors stabilizes intermediate structures, revealing a sequential activation mechanism. This finding explains how these receptors, crucial for synaptic communication, transition between inactive and active states.

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Area of Science:

  • Neuroscience
  • Structural Biology
  • Biochemistry

Background:

  • Postsynaptic receptors mediate synaptic communication by converting chemical signals to electrical responses.
  • Ligand-gated ion channels undergo conformational changes upon agonist binding, leading to channel opening and influencing postsynaptic signaling.

Purpose of the Study:

  • To elucidate the structural mechanisms underlying the activation of the muscle-type nicotinic acetylcholine receptor.
  • To determine the receptor's structures in unliganded, mono-liganded, and di-liganded states.

Main Methods:

  • High-resolution structural determination of the muscle-type nicotinic acetylcholine receptor.
  • Single-channel recordings to correlate structural states with functional activity.

Main Results:

  • Agonist binding to a single site induces a closed state where one subunit adopts an active-like conformation, while the other remains inactive.
  • An intermediate structure was identified, revealing asynchronous subunit transitions during receptor activation.

Conclusions:

  • The muscle-type nicotinic acetylcholine receptor activation proceeds via a sequential mechanism involving asynchronous subunit transitions.
  • This mechanism has implications for understanding the function of the broader superfamily of pentameric ligand-gated ion channels.