Neuromuscular junction: botulism: practice question

A Physiology 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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Physiology · Neuromuscular junction: botulism

Sample item

A 7-month-old infant fed honey has constipation, a weak cry, poor feeding and symmetrical descending flaccid weakness. What is the action of the responsible toxin?

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

The answer and the reasoning

C. Cleavage of SNARE proteins in the motor nerve terminal, preventing acetylcholine vesicle fusion

Botulinum toxin is a zinc protease that cleaves SNARE proteins such as SNAP-25 and synaptobrevin at the peripheral cholinergic nerve terminal. Acetylcholine vesicles cannot fuse with the membrane, so release stops and flaccid paralysis follows. Recovery needs regrowth of new terminals, and therapeutic doses are used for dystonia and spasticity.

Option by option

  • A. Blockade of glycine release from spinal inhibitory interneurons

    Blockade of glycine release from inhibitory interneurons is the action of tetanus toxin, causing spastic paralysis.

  • B. Inhibition of voltage-gated sodium channels in the axon

    Sodium channel blockade is the action of tetrodotoxin and local anaesthetics.

  • C. Cleavage of SNARE proteins in the motor nerve terminal, preventing acetylcholine vesicle fusion (correct)

    SNARE cleavage stops vesicle fusion and acetylcholine release.

  • D. Irreversible blockade of postsynaptic nicotinic receptors

    Postsynaptic receptor blockade is the action of curare-like agents and alpha-bungarotoxin, not botulinum toxin.

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 Physiology question

What is the answer to this Physiology question?

The best answer is C, Cleavage of SNARE proteins in the motor nerve terminal, preventing acetylcholine vesicle fusion. Botulinum toxin is a zinc protease that cleaves SNARE proteins such as SNAP-25 and synaptobrevin at the peripheral cholinergic nerve terminal.

Why is "Blockade of glycine release from spinal inhibitory interneurons" not the answer?

Blockade of glycine release from inhibitory interneurons is the action of tetanus toxin, causing spastic paralysis.

Why is "Inhibition of voltage-gated sodium channels in the axon" not the answer?

Sodium channel blockade is the action of tetrodotoxin and local anaesthetics.

Why is "Irreversible blockade of postsynaptic nicotinic receptors" not the answer?

Postsynaptic receptor blockade is the action of curare-like agents and alpha-bungarotoxin, not botulinum toxin.

What concept does this question test?

It tests Neuromuscular junction: botulism in Physiology. Acetylcholine vesicles cannot fuse with the membrane, so release stops and flaccid paralysis follows. Recovery needs regrowth of new terminals, and therapeutic doses are used for dystonia and spasticity.

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: botulism?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology 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.