Neuromuscular junction: botulinum toxin: practice question

A Pharmacology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Pharmacology · Neuromuscular junction: botulinum toxin

Sample item

A 45-year-old man with cervical dystonia receives botulinum toxin type A injections into the sternocleidomastoid, with relief for about three months. At the nerve terminal, what is the molecular action of the toxin?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Cleaves SNARE proteins such as SNAP-25, preventing acetylcholine vesicle fusion

Botulinum toxin is a zinc-dependent protease that is taken up into cholinergic terminals and cleaves SNARE proteins; type A cleaves SNAP-25. Without SNARE function, acetylcholine-containing vesicles cannot fuse with the membrane, causing flaccid paralysis until new terminals sprout. Clinical effect therefore wears off over months.

Option by option

  • A. Blocks postsynaptic nicotinic receptors competitively

    Competitive nicotinic receptor blockade is the mechanism of non-depolarising blockers such as vecuronium.

  • B. Inhibits choline uptake into the nerve terminal

    Inhibition of choline uptake is the action of hemicholinium, which is only an experimental tool.

  • C. Inhibits acetylcholinesterase at the junction

    Acetylcholinesterase inhibition would increase, not reduce, junctional acetylcholine and is the action of neostigmine.

  • D. Cleaves SNARE proteins such as SNAP-25, preventing acetylcholine vesicle fusion (correct)

    Cleavage of SNARE proteins abolishes exocytosis of acetylcholine, giving long-lasting chemodenervation.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Pharmacology question

What is the answer to this Pharmacology question?

The best answer is D, Cleaves SNARE proteins such as SNAP-25, preventing acetylcholine vesicle fusion. Botulinum toxin is a zinc-dependent protease that is taken up into cholinergic terminals and cleaves SNARE proteins; type A cleaves SNAP-25.

Why is "Blocks postsynaptic nicotinic receptors competitively" not the answer?

Competitive nicotinic receptor blockade is the mechanism of non-depolarising blockers such as vecuronium.

Why is "Inhibits choline uptake into the nerve terminal" not the answer?

Inhibition of choline uptake is the action of hemicholinium, which is only an experimental tool.

Why is "Inhibits acetylcholinesterase at the junction" not the answer?

Acetylcholinesterase inhibition would increase, not reduce, junctional acetylcholine and is the action of neostigmine.

What concept does this question test?

It tests Neuromuscular junction: botulinum toxin in Pharmacology. Without SNARE function, acetylcholine-containing vesicles cannot fuse with the membrane, causing flaccid paralysis until new terminals sprout. Clinical effect therefore wears off over months.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Neuromuscular junction: botulinum toxin?

Learn drugs as classes, then the exception in each class that an examiner would pick. Then use the flashcards and the other Pharmacology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.