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

6.5K
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...
6.5K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

4.7K
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
4.7K
Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

5.9K
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+....
5.9K
Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

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

2.5K
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...
2.5K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

4.7K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
4.7K
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

4.2K
The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
4.2K

You might also read

Related Articles

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

Sort by
Same author

Tyrosine kinase signaling pathways as therapeutic targets in autoimmune subepidermal blistering skin diseases (pemphigoid diseases).

Frontiers in immunology·2026
Same author

EULAR recommendations for the management of rheumatoid arthritis with synthetic and biologic disease-modifying antirheumatic drugs: 2025 update.

Annals of the rheumatic diseases·2026
Same author

Neutrophil deficiency increases T cell numbers at the site of tissue injury in mice.

FEBS letters·2025
Same author

Surgical Treatment of Multiple Bone Cysts Using a Platelet-Rich Fibrin and BoneAlbumin Composite Graft: A Case Report.

Reports (MDPI)·2025
Same author

Genetic Variants of the Human Thiamine Transporter (<i>SLC19A3</i>, THTR2)-Potential Relevance in Metabolic Diseases.

International journal of molecular sciences·2025
Same author

Time-restricted feeding alleviates arthritis symptoms augmented by high-fat diet.

Frontiers in immunology·2025

Related Experiment Video

Updated: Mar 24, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.4K

Nicotinic acetylcholine receptors modulate osteoclastogenesis.

Peter Mandl1, Silvia Hayer2, Thomas Karonitsch3

  • 1Division of Rheumatology, Medical University of Vienna, Vienna, Austria. peter.mandl@meduniwien.ac.at.

Arthritis Research & Therapy
|March 14, 2016
PubMed
Summary

Nicotinic acetylcholine receptors (nAChRs) significantly impact bone health by regulating osteoclast formation. Targeting nAChRs inhibits osteoclast activity and promotes bone volume, offering potential therapeutic avenues.

Keywords:
Acetylcholine receptorNicotineOsteoclastogenesis

More Related Videos

A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro
07:03

A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro

Published on: June 16, 2022

7.6K
A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

12.2K

Related Experiment Videos

Last Updated: Mar 24, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.4K
A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro
07:03

A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro

Published on: June 16, 2022

7.6K
A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

12.2K

Area of Science:

  • Bone Biology and Physiology
  • Neuropharmacology

Background:

  • Nicotinic acetylcholine receptors (nAChRs) are implicated in various physiological processes.
  • Their role in bone homeostasis and osteoclastogenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the function of nAChRs in in-vitro osteoclastogenesis.
  • To elucidate the role of nAChRs in in-vivo bone homeostasis.

Main Methods:

  • Osteoclastogenesis assays, RT-PCR, Western blot, and flow cytometry were used to study nAChR subunits and agonist effects.
  • Bone phenotype analysis in knockout mice involved pQCT and histomorphometry.
  • Intracellular calcium oscillations were measured using Fura-2 fluorescence.

Main Results:

  • nAChR subunits were detected in macrophages, which produced acetylcholine.
  • nAChR agonists dose-dependently reduced osteoclast formation and tartrate-resistant acidic phosphatase-positive cells.
  • Inhibition of RANKL-induced calcium oscillations and downstream signaling (NFATc1, c-fos) was observed.
  • Mice lacking α7 or β2-containing nAChRs showed reduced in-vitro osteoclastogenesis.
  • Male α7 nAChR knockout mice exhibited increased bone volume in vivo.

Conclusions:

  • nAChR activity significantly influences osteoclastogenesis in mice.
  • nAChR agonists inhibit osteoclast calcium oscillations and RANKL-induced signaling.
  • Reduced osteoclastogenesis in α7 knockout mice correlated with increased bone volume in vivo.