Related Experiment Video
Updated: Jun 8, 2026
04:30
Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models
Published on: March 8, 2024
Post-junctional interactions between neuromuscular blocking agents and ethanol at the mouse neuromuscular junction
1Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, Chicago, IL, USA. tjs026@northwestern.edu
British Journal of Pharmacology
|October 1, 2010
Summary
Ethanol enhances neuromuscular transmission by acting on post-synaptic elements and interacting with neuromuscular blockers. This may alter dosages of these drugs in patients who consume alcohol.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Ethanol affects the mammalian nervous system, including the neuromuscular junction.
- Previous studies have not investigated ethanol's effects on evoked synaptic transmission at the mouse neuromuscular junction.
Purpose of the Study:
- To investigate the effects of ethanol on evoked neuromuscular transmission.
- To examine ethanol's interaction with non-depolarizing blocking drugs at the neuromuscular junction.
Main Methods:
- Electrophysiological techniques were used to measure synaptic potentials and currents.
- Experiments were conducted on mouse neuromuscular junctions.
Main Results:
- Ethanol increased the amplitude of spontaneous and evoked synaptic events.
- Ethanol enhanced evoked responses more than spontaneous responses when neuromuscular transmission was blocked.
- Ethanol interfered with vecuronium but not cisatracurium neuromuscular blockade.
Conclusions:
- Ethanol's stimulant effect on neuromuscular transmission is post-junctional, enhancing nicotinic receptor transmission.
- Ethanol interacts with neuromuscular blocking agents, potentially affecting drug dosages.
- These findings have implications for managing patients who have consumed alcohol and require neuromuscular blockade.
More Related Videos
Related Concept Videos
01:29Neuromuscular 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...
01:27Nondepolarizing (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...
Although all competitive neuromuscular blockers are designed...
01:17Nondepolarizing (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...
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
01:11Nondepolarizing (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...
Instead, they are transported by the blood to different tissues. Muscles with a greater blood supply (arteries) and blood flow receive more...
01:28Depolarizing 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...
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...
01:19Depolarizing 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...