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

Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

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...
Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

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

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...
Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

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+. Activation...
Cholinergic Antagonists: Chemistry and Structure-Activity Relationship01:29

Cholinergic Antagonists: Chemistry and Structure-Activity Relationship

Cholinergic antagonists bind to cholinergic receptors and limit the effects of acetylcholine and other cholinergic agonists. Based on the specific cholinergic receptor affinity, these antagonists are classified as muscarinic or nicotinic. Anticholinergics interrupt parasympathetic innervations while sympathetic innervations remain uninterrupted. Muscarinic antagonists are also called 'muscarinic antagonists', 'antimuscarinics', or 'parasympatholytics'. Nicotinic antagonists are called...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Correction: Cognitive synaptopathy: synaptic and dendritic spine dysfunction in age-related cognitive disorders.

Frontiers in aging neuroscience·2026
Same author

Machine Learning in Single-Molecule Tracking Analysis of Superresolution Optical Microscopy Data.

Cells·2026
Same author

Synapse-associated neuropathological markers in Alzheimer disease.

Brain : a journal of neurology·2026
Same author

Quantitative evaluation of methods to analyze motion changes in single-particle experiments.

Nature communications·2025
Same author

Concurrent diffusion of nicotinic acetylcholine receptors and fluorescent cholesterol disclosed by two-colour sub-millisecond MINFLUX-based single-molecule tracking.

Nature communications·2025
Same author

Nicotinic acetylcholine receptors in the brain.

Handbook of clinical neurology·2025

Related Experiment Video

Updated: Jul 10, 2026

Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells
09:06

Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells

Published on: December 19, 2025

Cholesterol effects on nicotinic acetylcholine receptor.

Francisco J Barrantes1

  • 1Instituto de Investigaciones Bioquímicas de Bahía Blanca, Bahía Blanca, Argentina. rtfjb1@criba.edu.ar

Journal of Neurochemistry
|December 6, 2007
PubMed
Summary

Cholesterol significantly impacts acetylcholine receptor (AChR) organization and function. Lowering cholesterol increases AChR channel activity and alters nanocluster distribution, affecting cell surface stability.

More Related Videos

Utilizing pHluorin-tagged Receptors to Monitor Subcellular Localization and Trafficking
09:59

Utilizing pHluorin-tagged Receptors to Monitor Subcellular Localization and Trafficking

Published on: March 16, 2017

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
10:48

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

Published on: January 25, 2019

Related Experiment Videos

Last Updated: Jul 10, 2026

Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells
09:06

Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells

Published on: December 19, 2025

Utilizing pHluorin-tagged Receptors to Monitor Subcellular Localization and Trafficking
09:59

Utilizing pHluorin-tagged Receptors to Monitor Subcellular Localization and Trafficking

Published on: March 16, 2017

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
10:48

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

Published on: January 25, 2019

Area of Science:

  • Biophysics
  • Cell Biology
  • Neuroscience

Background:

  • Cholesterol (Chol) plays a crucial role in modulating the structure and function of cell membrane proteins.
  • The muscle-type nicotinic acetylcholine receptor (AChR) is essential for neuromuscular transmission and its regulation by cholesterol is under investigation.

Purpose of the Study:

  • To investigate the effects of cholesterol on the stability, supramolecular organization, and function of the murine muscle-type nicotinic acetylcholine receptor (AChR).
  • To elucidate the biophysical properties of cholesterol-AChR interactions and their impact on receptor behavior.

Main Methods:

  • Utilized a receptor-expressing clonal cell line and advanced microscopy techniques, including stimulated emission depletion (STED) fluorescence microscopy.
  • Employed Ripley's K-test to analyze nanocluster distribution and cytoskeletal interactions.

Main Results:

  • Acute cholesterol depletion reduced AChR aggregates by ~50% via accelerated endocytosis.
  • Cholesterol depletion led to ion channel gain-of-function, while enrichment had the opposite effect.
  • Cholesterol affects the short- and long-range organization of AChR nanoclusters, altering their size and distribution.

Conclusions:

  • Cholesterol content homeostatically modulates cell-surface organization and stability of AChR nanodomains.
  • Cholesterol fine-tunes AChR channel function, potentially compensating for acute receptor loss.
  • Findings support the 'raft' hypothesis regarding cholesterol's role in membrane microdomains.