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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...
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Botulism is a life-threatening neuroparalytic condition caused by botulinum neurotoxin, which is produced by the bacterium Clostridium botulinum, a Gram-positive, spore-forming, obligate anaerobe.In adults, the toxin enters the body in different ways: in foodborne botulism, the preformed toxin is absorbed in the intestine. In wound botulism, spores grow in injured tissue and release the toxin into the blood. Infant botulism differs mechanistically from adult forms. In infants, botulism commonly...
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.
The binding of dantrolene to the RYR1...
Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Tetanus01:29

Tetanus

Tetanus is a life-threatening neurological disorder characterized by persistent muscle contractions and spastic paralysis. It is caused by Clostridium tetani, a motile, Gram-positive, rod-shaped, obligate anaerobe. These bacteria produce terminal endospores, giving them a distinctive “lollipop” or “tennis-racket” appearance. They thrive in anaerobic environments, such as those found in deep puncture wounds.Once introduced into the body, the spores germinate into vegetative cells. These cells...
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...

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Loading a Calcium Dye into Frog Nerve Endings Through the Nerve Stump: Calcium Transient Registration in the Frog Neuromuscular Junction
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Loading a Calcium Dye into Frog Nerve Endings Through the Nerve Stump: Calcium Transient Registration in the Frog Neuromuscular Junction

Published on: July 8, 2017

Frontoxins, three-finger toxins from Micrurus frontalis venom, decrease miniature endplate potential amplitude at

K G Moreira1, M V Prates, F A C Andrade

  • 1Universidade de Brasília - Pós-graduação em Biologia Animal, Brasília-DF, Brazil.

Toxicon : Official Journal of the International Society on Toxinology
|March 25, 2010
PubMed
Summary
This summary is machine-generated.

Six new Frontoxins (FTx) from Brazilian coral snake venom were sequenced. These toxins, similar to alpha-neurotoxins, block nicotinic acetylcholine receptors, explaining snakebite neurotoxicity.

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Registration of Calcium Transients in Mouse Neuromuscular Junction with High Temporal Resolution using Confocal Microscopy
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Registration of Calcium Transients in Mouse Neuromuscular Junction with High Temporal Resolution using Confocal Microscopy

Published on: December 1, 2021

Area of Science:

  • Biochemistry
  • Toxicology
  • Neuroscience

Background:

  • Brazilian coral snake (Micrurus frontalis) venom causes neurotoxicity.
  • Limited M. frontalis venom availability has hindered neurotoxin sequencing.

Purpose of the Study:

  • To isolate, purify, and sequence novel neurotoxins from M. frontalis venom.
  • To characterize the structure and function of these new toxins.

Main Methods:

  • Isolation of toxins using reversed-phase high-performance liquid chromatography (RP-HPLC).
  • Mass determination via MALDI-TOF and ESI ion-trap mass spectrometry.
  • Amino acid sequencing using Edman degradation and de novo sequencing.

Main Results:

  • Six new three-finger like toxins, named Frontoxin (FTx) I-VI, were identified.
  • FTx II, III, IV, and V were fully sequenced.
  • FTx I, II, III, and VI resemble short-chain alpha-neurotoxins; FTx IV and V resemble long-chain alpha-neurotoxins.
  • FTx II, III, and IV reduced miniature endplate potential amplitudes in frog neuromuscular junctions.

Conclusions:

  • Frontoxins (FTx) are novel neurotoxins from M. frontalis venom.
  • These toxins likely block nicotinic acetylcholine receptors, contributing to envenomation neurotoxicity.