Related Experiment Video

Updated: Aug 13, 2026

Measuring Spinal Presynaptic Inhibition in Mice By Dorsal Root Potential Recording In Vivo
09:48

Measuring Spinal Presynaptic Inhibition in Mice By Dorsal Root Potential Recording In Vivo

Published on: March 29, 2014

Effect of prednisolone on neuromuscular blocking in mice in vivo

W F Arts, H J Oosterhuis

    Neurology
    |November 1, 1975
    PubMed

    Insights

    Prednisolone partially or fully reversed the neuromuscular blocking effects of d-tubocurarine and hemicholinium-3 in mice. This suggests a potential mechanism for prednisone's benefit in myasthenia gravis treatment.

    Area of Science:

    • Pharmacology
    • Neuroscience
    • Muscle Physiology

    Background:

    • Neuromuscular blocking agents like d-tubocurarine and hemicholinium-3 are used in research and medicine.
    • Myasthenia gravis is a condition characterized by neuromuscular weakness, often treated with prednisone.
    • The interaction between corticosteroids and neuromuscular blockers requires further elucidation.

    Purpose of the Study:

    • To investigate the effect of prednisolone on the neuromuscular blocking action of d-tubocurarine and hemicholinium-3.
    • To explore potential mechanisms underlying prednisone's therapeutic effects in myasthenia gravis.

    Main Methods:

    • Inbred female Swiss mice were used to assess working capacity on a rotating rod.
    • Mice were pre-injected with prednisolone (1.2 mg) before administration of d-tubocurarine or hemicholinium-3.
    • Neuromuscular blocking effects were evaluated based on performance on the rotating rod.

    Main Results:

    • Prednisolone demonstrated the ability to partially or wholly antagonize the neuromuscular blocking effects of both d-tubocurarine and hemicholinium-3.
    • The degree of antagonism varied depending on the specific neuromuscular blocker and dose used.

    Conclusions:

    • Prednisolone exhibits an antagonistic effect on neuromuscular blockade induced by d-tubocurarine and hemicholinium-3.
    • These findings provide a potential pharmacological explanation for the clinical efficacy of prednisone in managing myasthenia gravis symptoms.

    More Related Videos

    In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration06:35

    In Vivo Electrophysiological Measurement of Compound Muscle Action Potential from the Forelimbs in Mouse Models of Motor Neuron Degeneration

    Published on: June 15, 2018

    Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models04:30

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

    Published on: March 8, 2024

    Related Concept Videos

    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...
    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...
    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: 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...
    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...
    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...