Wed20October0612PM 2

Acetylcholine release at the neuromuscular junction is:

True / False

Increased by tetanic stimulation Correct

Decreased by botulinum toxin Incorrect answer selected

Inhibited by 4-aminopyridine Incorrect answer selected

Increased by lithium Correct

Decreased by aminoglycosides Correct

Explanation

Lithium can prolong the effects of non-depolarising and depolarising neuromuscular blockade. This is thought to be due to inhibition of synthesis and release of acetylcholine (Ach) at the neuromuscular junction.

The aminoglycoside class of antibiotics can produce neuromuscular blockade in the absence of muscle relaxants. They have been shown to cause a pre-junctional, magnesium-like depression of Ach release. Potentiation of non-depolarising neuromuscular blocking agents has been reported, in particular vecuronium.

A tetanic stimulus of 50-100 Hz applied to a nerve supplying skeletal muscle results in the mobilisation and release of Ach stores. This forms the basis of post-tetanic facilitation that characterises non-depolarising neuromuscular blockade.

4-aminopyridine is a drug that blocks potassium channels in neurones and as a result improves the transmission of impulses down damaged axons. It is used in patients with multiple sclerosis to improve symptoms. Apart from an increase in conduction speed, increased neurotransmitter release and an increase in the number of synaptic terminals activated may account for improvement in muscle power.

Botulinum toxin (BT) is a potent neurotoxin produced by the

bacterium Clostridium botulinum. There are seven sero-subtypes (A, B, C, D, E, F and G) all of which bind to extracellular glycoproteins on cholinergic nerve terminals and block presynaptic acetylcholine release.

Answer Statistics

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Average score: 69.58%

Times answered: 236