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

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

729
Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...
729
Indirect-Acting Cholinergic Agonists: Mechanism of Action01:18

Indirect-Acting Cholinergic Agonists: Mechanism of Action

2.0K
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,...
2.0K
Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

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

635
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.
Reversible inhibitors display short to medium durations of action. Short-acting agents include simple alcohols with...
635
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

1.7K
Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
1.7K
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

2.0K
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...
2.0K
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

3.4K
The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
3.4K

You might also read

Related Articles

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

Sort by
Same author

Migraine and menopause as converging factors in brain vulnerability: a hypothesis-driven perspective.

The journal of headache and pain·2026
Same author

Opportunities and Concerns of Gamified, Extended Reality for Home-Based Motor Rehabilitation for Children With Brain Injury: Qualitative Case Study on Design Elements Related to the Engagement and Fatigue Perspectives.

Journal of medical Internet research·2026
Same author

Bridging digital health gaps in South Africa: A qualitative study of the digital divide, interoperability and health equity.

Digital health·2026
Same author

Exploring Stakeholders' Perceptions of Using Digital Health Technologies to Improve the Conservative Treatment of Adolescent Idiopathic Scoliosis: Qualitative Study.

Journal of medical Internet research·2025
Same author

Identification of required capabilities of digital health ecosystems when preventing and managing non-communicable diseases.

Digital health·2024
Same author

Social Media Use and Consumption of Prescription-Free Medications for Anxiety, Sleep, and Pain among Norwegian University Students.

European journal of investigation in health, psychology and education·2024

Related Experiment Video

Updated: Aug 24, 2025

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors
04:59

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors

Published on: September 27, 2019

12.3K

How Does Botulinum Toxin Inhibit Itch?

Parisa Gazerani1,2

  • 1Department of Life Sciences and Health, Faculty of Health Sciences, Oslo Metropolitan University, 0130 Oslo, Norway.

Toxins
|October 26, 2022
PubMed
Summary

Botulinum neurotoxins (BoNTs) show potential for treating itch, but more rigorous clinical trials are needed. Understanding the mechanisms of action, including neuronal and immune modulation, can accelerate the approval of BoNTs for itchy conditions.

Keywords:
anti-pruriticbotulinum neurotoxinitchmechanism of action

More Related Videos

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
10:30

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators

Published on: December 27, 2013

5.4K
A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
14:10

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors

Published on: November 14, 2014

8.7K

Related Experiment Videos

Last Updated: Aug 24, 2025

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors
04:59

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors

Published on: September 27, 2019

12.3K
A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators
10:30

A High-throughput-compatible FRET-based Platform for Identification and Characterization of Botulinum Neurotoxin Light Chain Modulators

Published on: December 27, 2013

5.4K
A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
14:10

A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors

Published on: November 14, 2014

8.7K

Area of Science:

  • Neuroscience
  • Dermatology
  • Pharmacology

Background:

  • Botulinum neurotoxins (BoNTs) have demonstrated anti-pruritic effects, yet lack regulatory approval for anti-itch indications.
  • Current evidence relies heavily on off-label use and case studies, with limited randomized clinical trials yielding controversial results.
  • Higher levels of evidence, including large-scale, well-designed studies, are necessary for BoNTs to gain approval for treating pruritic conditions.

Purpose of the Study:

  • To review the current state of knowledge on the mechanisms underlying the anti-itch effects of BoNTs.
  • To consolidate evidence from basic research on how BoNTs modulate neuronal, glial, and immune pathways involved in itch transmission.
  • To outline future research directions to support the development and approval of BoNTs for itchy conditions.

Main Methods:

  • Systematic review of basic science studies investigating the mechanisms of BoNTs' anti-pruritic action.
  • Analysis of evidence for neuronal, glial, and immune modulatory effects of BoNTs relevant to itch.
  • Identification of knowledge gaps and future research priorities.

Main Results:

  • BoNTs exhibit anti-itch effects through modulation of neuronal signaling, glial cell activity, and immune responses.
  • Evidence suggests BoNTs can interfere with the transmission of itch signals at various levels.
  • The underlying mechanisms provide a scientific basis for the observed clinical benefits in pruritic conditions.

Conclusions:

  • Understanding the multifaceted mechanisms of BoNTs' anti-itch action is crucial for advancing their clinical application.
  • Further research focusing on well-designed clinical trials and mechanistic studies is warranted.
  • Consolidating mechanistic insights can accelerate the pathway towards regulatory approval for BoNTs in treating itchy conditions.