Related Experiment Video

Updated: Sep 7, 2026

Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models
04:30

Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models

Published on: March 8, 2024

Action of bretylium and guanethidine at the neuromuscular junction

B N DIXIT, O D GULATI, S D GOKHALE

    British Journal of Pharmacology and Chemotherapy
    |December 1, 1961
    PubMed

    Keywords:
    AMIDINES/pharmacologyANTIHYPERTENSIVE AGENTS/pharmacologyMYONEURAL JUNCTION/pharmacology

    More Related Videos

    Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology10:26

    Bladder Smooth Muscle Strip Contractility as a Method to Evaluate Lower Urinary Tract Pharmacology

    Published on: August 18, 2014

    Subcutaneous Administration of Muscarinic Antagonists and Triple-Immunostaining of the Levator Auris Longus Muscle in Mice07:09

    Subcutaneous Administration of Muscarinic Antagonists and Triple-Immunostaining of the Levator Auris Longus Muscle in Mice

    Published on: September 8, 2011

    Related Concept Videos

    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...
    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...
    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...
    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...
    Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics01:11

    Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics

    All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
    Instead, they are transported by the blood to different tissues. Muscles with a greater blood supply (arteries) and blood flow receive more...