Neuromuscular junction: 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

Sample item

A patient given tubocurarine during surgery shows muscle paralysis. At the neuromuscular junction, what is the primary effect?

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

The answer and the reasoning

A. Competitive blockade of nicotinic receptors, so the end-plate potential fails to reach threshold

Tubocurarine competes with acetylcholine at the postsynaptic nicotinic receptor and reduces the end-plate potential below the threshold needed to trigger a muscle action potential. Anticholinesterases can reverse it by raising acetylcholine concentration.

Option by option

  • A. Competitive blockade of nicotinic receptors, so the end-plate potential fails to reach threshold (correct)

    Correct. This is competitive non-depolarising blockade.

  • B. Inhibition of acetylcholinesterase

    Cholinesterase inhibition would prolong, not block, transmission.

  • C. Persistent depolarisation of the end plate

    Persistent end-plate depolarisation is the mechanism of suxamethonium.

  • D. Inhibition of acetylcholine release from the nerve terminal

    Inhibition of release is the mechanism of 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 A, Competitive blockade of nicotinic receptors, so the end-plate potential fails to reach threshold. Tubocurarine competes with acetylcholine at the postsynaptic nicotinic receptor and reduces the end-plate potential below the threshold needed to trigger a muscle action potential.

Why is "Inhibition of acetylcholinesterase" not the answer?

Cholinesterase inhibition would prolong, not block, transmission.

Why is "Persistent depolarisation of the end plate" not the answer?

Persistent end-plate depolarisation is the mechanism of suxamethonium.

Why is "Inhibition of acetylcholine release from the nerve terminal" not the answer?

Inhibition of release is the mechanism of botulinum toxin.

What concept does this question test?

It tests Neuromuscular junction in Physiology. Anticholinesterases can reverse it by raising acetylcholine concentration.

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?

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.