18 Questions
What type of inhibition is seen with triethylcholine?
Competitive inhibition
Which ion is involved in the blockade of Ca2+-mediated exocytosis of synaptic vesicle?
Mg2+
What is the mechanism of action of botulinum toxin?
Inhibition of SNARE proteins
What is the effect of β-bungarotoxin on the neuromuscular junction?
Hydrolysis of membrane phospholipids
What is the primary use of drugs that enhance ACh transmission in the context of botulinum toxin?
Ineffective due to irreversible action
What type of blockers are structural analogues of acetylcholine?
Postsynaptic blockers
What is the primary function of acetylcholinesterase (AChE) in the neuromuscular junction?
To break down acetylcholine into inactive components
How many synaptic vesicles are typically released by a single nerve impulse in the neuromuscular junction?
300
What is the site of action for drugs that inhibit acetylcholine synthesis and release?
Motor neuron terminal
What is the primary mechanism of pharmacological blockade of the neuromuscular junction?
Blockade of nicotinic receptors
What is the primary function of the nicotinic receptor in the neuromuscular junction?
To bind and respond to acetylcholine released from motor neurons
How long do acetylcholine molecules interact with nicotinic receptors in the neuromuscular junction?
2 milliseconds
What happens to sodium in the ion channel when a depolarizing neuromuscular blocker is used?
It is blocked from entering the cell
Why do patients with muscle denervation have an increased risk of heart dysrhythmia or arrest when using depolarizing blockers?
Due to hyperkalemia
What is the main difference between depolarizing and non-depolarizing blockers?
Depolarizing blockers are non-competitive inhibitors, while non-depolarizing blockers are competitive
What is the primary mechanism of action of suxamethonium?
Depolarizing the muscle fiber
Why is suxamethonium used during anesthesia induction?
To facilitate intubation
What is a rare but potential side effect of using suxamethonium?
Malignant hyperthermia
Study Notes
Pharmacological Blockade of the Neuromuscular Junction (NMJ)
Inhibitors of ACh Synthesis and Release
- Hemicholinium: blocks choline transporter, competitive inhibition
- Triethylcholine: blocks ACh synthesis, competitive inhibition, transported into terminal and converted into false neurotransmitter
- Vesamicol: inhibits ACh transport into synaptic vesicle
Inhibitors of ACh Release
- Mg2+: blocks Ca2+-mediated exocytosis of synaptic vesicle
- Aminoglycoside antibiotics (streptomycin, neomycin): specific block of ACh release
- Botulinum toxin (Botox): inactivates SNARE proteins required for exocytosis, high potency, causes botulism, used for relief of muscle spasm, eyelid spasm, and wrinkle removal
- β-Bungarotoxin: hydrolyses membrane phospholipids
Postsynaptic Neuromuscular Blockers
- Act as antagonists (non-depolarizing blockers) or agonists (depolarizing blockers) at nicotinic receptors
- Used during surgery to promote complete muscle relaxation without higher doses of anaesthetic
Depolarizing (Non-Competitive) Neuromuscular Blockers
- Cause continued depolarization leading to repolarization and block of sodium channel
- Prevent further depolarization, leading to twitching becoming flaccid paralysis
- Muscle twitching is short-lived
- No ganglionic block, except at very high doses
- Side effects: bradycardia, post-operative muscle pain, apnea, hyperkalemia, increased intraocular pressure, prolonged paralysis, and malignant hyperthermia
This quiz covers the key components of the neuromuscular junction and various drug strategies for modulating its function. Topics include neuromuscular junction blockade and its pharmacological applications. Assess your knowledge of neuropharmacology and pharmacology in this lecture-based quiz.
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