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

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

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...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

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...
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

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 succinylcholine...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...

You might also read

Related Articles

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

Sort by
Same author

Critically Ill Children Show Disrupted Sleep Patterns and Atypical Electroencephalograms: An Observational Cohort Study.

Acta paediatrica (Oslo, Norway : 1992)·2026
Same author

Feasibility and agreement of a self-adhesive EEG electrode set versus conventional EEG in postanoxic coma.

Resuscitation·2026
Same author

Motor Unit Patterns Correlate With Severity in Symptomatic Patients With Spinal Muscular Atrophy.

European journal of neurology·2025
Same author

Supervised machine learning on electrocardiography features to classify sleep in noncritically ill children.

Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine·2024
Same author

An electroencephalography-based sleep index and supervised machine learning as a suitable tool for automated sleep classification in children.

Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine·2023
Same author

Longitudinal prospective cohort study to assess peripheral motor function with extensive electrophysiological techniques in patients with Spinal Muscular Atrophy (SMA): the SMA Motor Map protocol.

BMC neurology·2023

Related Experiment Video

Updated: Jun 7, 2026

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
09:34

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Published on: August 27, 2019

Activity-dependent conduction block in chronic inflammatory demyelinating polyneuropathy.

Dirk C G Straver1, Leonard H van den Berg, Hessel Franssen

  • 1Neuromuscular Disease Group, Department of Neurology and Clinical Neurophysiology, Rudolf Magnus Institute for Neuroscience, University Medical Centre Utrecht, PO Box 85500 3508 GA Utrecht, The Netherlands.

Journal of the Neurological Sciences
|November 2, 2010
PubMed
Summary

Activity-dependent conduction block (CB) does not cause weakness in chronic inflammatory demyelinating polyneuropathy (CIDP). Muscle activity in CIDP patients increases temporal dispersion, not conduction block, suggesting new therapeutic targets.

More Related Videos

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat
08:05

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat

Published on: November 21, 2025

Recording Network Activity in Spinal Nociceptive Circuits Using Microelectrode Arrays
11:28

Recording Network Activity in Spinal Nociceptive Circuits Using Microelectrode Arrays

Published on: February 9, 2022

Related Experiment Videos

Last Updated: Jun 7, 2026

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
09:34

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Published on: August 27, 2019

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat
08:05

Electrophysiological Methods to Assess Peripheral Pain Block in an Anesthetized Rat

Published on: November 21, 2025

Recording Network Activity in Spinal Nociceptive Circuits Using Microelectrode Arrays
11:28

Recording Network Activity in Spinal Nociceptive Circuits Using Microelectrode Arrays

Published on: February 9, 2022

Area of Science:

  • Neurology
  • Neurophysiology
  • Clinical Electrophysiology

Background:

  • Activity-dependent conduction block (CB) was previously suggested to cause weakness in chronic inflammatory demyelinating polyneuropathy (CIDP).
  • Prior studies had limitations including single nerve segment analysis, submaximal stimulation, and exclusion of nerves with very low compound muscle action potentials (CMAPs).
  • Establishing robust evidence for activity-dependent CB is crucial as it represents a potential pharmacological treatment target.

Purpose of the Study:

  • To rigorously investigate the presence and extent of activity-dependent conduction block (CB) in chronic inflammatory demyelinating polyneuropathy (CIDP) using standardized criteria.
  • To determine if muscle activity, specifically maximal voluntary contraction (MVC), induces CB in CIDP patients.

Main Methods:

  • Evaluated 22 nerve segments in 18 CIDP patients using supramaximal electrical stimulation.
  • Assessed nerve conduction before and after 60 seconds of maximal voluntary contraction (MVC).
  • Calculated segmental and total area ratios to quantify conduction block, excluding nerves with markedly reduced CMAPs.

Main Results:

  • Maximal voluntary contraction (MVC) did not induce significant changes in mean area ratios, indicating minimal to no activity-dependent conduction block (CB) across tested segments.
  • MVC led to increased distal and proximal compound muscle action potential (CMAP) area and duration.
  • In demyelinative segments, MVC increased CMAP duration prolongation, suggesting increased temporal dispersion rather than CB.

Conclusions:

  • Muscle activity in chronic inflammatory demyelinating polyneuropathy (CIDP) does not induce significant activity-dependent conduction block (CB).
  • Maximal voluntary contraction (MVC) primarily increases temporal dispersion of nerve action potentials in CIDP.
  • Findings challenge the role of activity-dependent CB in CIDP weakness and suggest focusing on temporal dispersion for therapeutic strategies.