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Related Concept Videos

Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

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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.
There are two types of nicotinic receptors: neuromuscular (NM/NM/N1) and neuronal (NN/NN/N2). The two families differ based on their location and selectivity to...
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Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

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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. 
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+....
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Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

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

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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.
The direct-acting...
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Cholinergic Neurons: Neurotransmission01:23

Cholinergic Neurons: Neurotransmission

5.7K
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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Parasympathetic Signaling01:30

Parasympathetic Signaling

3.6K
Parasympathetic signaling plays a crucial role in regulating various physiological processes. It involves the release of acetylcholine (ACh) by parasympathetic neurons, which can have localized and short-lived effects. The majority of ACh released is rapidly inactivated at the synapse by the enzyme acetylcholinesterase (AChE), which hydrolyzes Ach into choline and acetate. Additionally, the tissue cholinesterase deactivates any ACh diffusing into the surrounding tissues.
The effects of...
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Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

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Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
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Related Experiment Video

Updated: Mar 3, 2026

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine

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NACHO Mediates Nicotinic Acetylcholine Receptor Function throughout the Brain.

Jose A Matta1, Shenyan Gu1, Weston B Davini1

  • 1Neuroscience Discovery, Janssen Pharmaceutical Companies of Johnson & Johnson, 3210 Merryfield Row, San Diego, CA 92121, USA.

Cell Reports
|April 27, 2017
PubMed
Summary

NACHO acts as a crucial chaperone for neuronal nicotinic acetylcholine receptors (nAChRs), facilitating their assembly and surface expression. This protein is essential for nAChR function, impacting brain activity and behavior.

Keywords:
Alzheimer’sNACHORIC3acetylcholinechaperonelearningnicotinereceptorsynapse

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Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
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Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Neuronal nicotinic acetylcholine receptors (nAChRs) are vital for brain function, behavior, and nicotine addiction.
  • nAChRs are assembled from various alpha and beta subunits, a process requiring strict regulation.
  • NACHO was previously identified as a specific chaperone for the alpha7 subtype of nAChRs.

Purpose of the Study:

  • To investigate the broader role of NACHO in the assembly of various neuronal nicotinic acetylcholine receptor subtypes.
  • To determine NACHO's function in the intracellular assembly and surface expression of nAChRs.
  • To assess the physiological and behavioral consequences of NACHO deficiency in vivo.

Main Methods:

  • Utilized NACHO knockout mouse models.
  • Assessed nAChR subunit assembly and surface expression.
  • Examined binding sites for specific nAChR ligands (α-bungarotoxin, epibatidine, conotoxin MII).
  • Evaluated locomotor and cognitive behaviors in knockout mice.

Main Results:

  • NACHO mediates the assembly of multiple major nAChR classes, not just the α7 subtype.
  • NACHO functions early in intracellular assembly and collaborates with RIC-3 for surface expression.
  • NACHO knockout mice exhibit significant deficits in binding sites for key nAChR ligands, indicating impaired assembly of α7-, α4β2-, and α6-containing nAChRs.
  • GABAA receptors remained unaffected, confirming NACHO's specificity for nAChRs.
  • NACHO deficiency led to behavioral abnormalities in locomotor activity and cognition.

Conclusions:

  • NACHO is a critical chaperone essential for the proper assembly and function of diverse neuronal nicotinic acetylcholine receptors.
  • NACHO plays a fundamental role in regulating nAChR expression and is crucial for normal brain physiology and behavior.
  • NACHO deficiency results in nAChR-related deficits, highlighting its importance in neurological function and potential therapeutic targeting for nAChR-associated diseases.