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Related Concept Videos

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

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.
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Skeletal Muscle Relaxants: Therapeutic Uses01:31

Skeletal Muscle Relaxants: Therapeutic Uses

Skeletal muscle relaxants are used to relax muscle tone and alleviate painful muscle contractions. However, the choice of skeletal muscle relaxants depends on the duration of the surgical procedure in order to minimize potential side effects. Skeletal muscle relaxants like neuromuscular blocking agents [NMBAs] are commonly employed as adjuvants alongside general anesthetics in clinical settings. NMBAs are also used to maintain controlled ventilation during surgery of the larynx or pharynx as...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

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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...
Depolarizing Blockers: Pharmocokinetics01:19

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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...
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Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
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Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

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Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...

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A High Content Imaging Assay for Identification of Botulinum Neurotoxin Inhibitors
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SNARE-wedging polyphenols as small molecular botox.

Yoosoo Yang1, Jin Kyu Choi, Chang Hwa Jung

  • 1School of Life Science and Biotechnology and Center for Human Interface Nano Technology, Sungkyunkwan University, Gyeonggi-do, Korea.

Planta Medica
|November 24, 2011
PubMed
Summary

Polyphenols like myricetin can paralyze muscles by inhibiting acetylcholine release, similar to botulinum neurotoxin (BoNT). These compounds offer a potentially safer alternative for treating hypersecretion diseases.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Clostridium botulinum neurotoxin (BoNT) applications rely on muscle paralysis via neurotransmitter release inhibition.
  • BoNT targets SNARE proteins, impairing neuroexocytosis at nerve terminals.
  • Polyphenols were previously shown to inhibit neurotransmitter release by disrupting SNARE complex formation.

Purpose of the Study:

  • To investigate the muscle paralyzing effects of myricetin, delphinidin, and cyanidin.
  • To determine if these polyphenols inhibit acetylcholine release at the neuromuscular junction.
  • To assess the safety and efficacy of myricetin as a potential therapeutic agent.

Main Methods:

  • In vitro studies on neuronal PC12 cells to assess neurotransmitter release inhibition.
  • In vivo studies to evaluate muscle paralysis and acetylcholine release inhibition.
  • Administration of myricetin at high doses (1000 mg/kg) to mice to assess toxicity.

Main Results:

  • Myricetin, delphinidin, and cyanidin were confirmed to paralyze muscle by inhibiting acetylcholine release.
  • Myricetin demonstrated a modest effect compared to BoNT/A but with a faster response time.
  • High-dose myricetin (1000 mg/kg) in mice did not result in mortality, indicating a favorable safety profile.

Conclusions:

  • Myricetin, delphinidin, and cyanidin show potential as therapeutic agents for hypersecretion diseases.
  • These polyphenols may offer a safer alternative to BoNT/A for conditions involving excessive secretion.
  • Further research is warranted to explore the full therapeutic potential of these compounds.