Nerve and muscle: magnesium and neuromuscular transmission: 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 · Nerve and muscle: magnesium and neuromuscular transmission

Sample item

A woman with pre-eclampsia receiving intravenous magnesium sulphate loses her knee-jerk reflexes. How does high extracellular magnesium reduce neuromuscular transmission?

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

The answer and the reasoning

D. It competes with calcium at presynaptic calcium channels, reducing acetylcholine release

Magnesium competes with calcium at presynaptic voltage-gated calcium channels, so each impulse releases fewer vesicles and the end-plate potential falls. Loss of tendon reflexes is the clinical sign of magnesium toxicity, warning of progression to respiratory depression.

Option by option

  • A. It prevents synthesis of acetylcholine in the terminal

    Acetylcholine synthesis is not prevented by magnesium.

  • B. It inhibits acetylcholinesterase, causing depolarisation block

    Magnesium does not inhibit acetylcholinesterase.

  • C. It blocks nicotinic receptors at the motor end plate irreversibly

    Magnesium does not irreversibly block nicotinic receptors; its action is mainly presynaptic.

  • D. It competes with calcium at presynaptic calcium channels, reducing acetylcholine release (correct)

    Correct. Reduced calcium entry means fewer quanta of acetylcholine are released.

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 D, It competes with calcium at presynaptic calcium channels, reducing acetylcholine release. Magnesium competes with calcium at presynaptic voltage-gated calcium channels, so each impulse releases fewer vesicles and the end-plate potential falls.

Why is "It prevents synthesis of acetylcholine in the terminal" not the answer?

Acetylcholine synthesis is not prevented by magnesium.

Why is "It inhibits acetylcholinesterase, causing depolarisation block" not the answer?

Magnesium does not inhibit acetylcholinesterase.

Why is "It blocks nicotinic receptors at the motor end plate irreversibly" not the answer?

Magnesium does not irreversibly block nicotinic receptors; its action is mainly presynaptic.

What concept does this question test?

It tests Nerve and muscle: magnesium and neuromuscular transmission in Physiology. Loss of tendon reflexes is the clinical sign of magnesium toxicity, warning of progression to respiratory depression.

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 Nerve and muscle: magnesium and neuromuscular transmission?

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.