Nerve and muscle: presynaptic inhibition: 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: presynaptic inhibition

Sample item

In the dorsal horn, an axo-axonal GABAergic synapse onto a primary afferent terminal reduces transmitter release without changing the postsynaptic membrane potential. How does it act?

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

The answer and the reasoning

B. It partly depolarises the terminal, reducing spike amplitude and calcium entry

In presynaptic inhibition, GABA acting on terminals with high intracellular chloride depolarises them modestly. This inactivates some sodium channels, reduces the amplitude of the arriving spike and so the calcium entry that triggers release, while the postsynaptic cell itself is not hyperpolarised.

Option by option

  • A. It cleaves SNARE proteins and blocks vesicle fusion

    Cleavage of SNARE proteins is the mechanism of botulinum and tetanus toxins.

  • B. It partly depolarises the terminal, reducing spike amplitude and calcium entry (correct)

    Correct. Terminal depolarisation shrinks the spike and the calcium signal for release.

  • C. It hyperpolarises the postsynaptic membrane through chloride entry

    Hyperpolarising the postsynaptic membrane is postsynaptic inhibition.

  • D. It speeds reuptake of the transmitter from the cleft

    Faster reuptake would shorten transmitter action but is not how axo-axonal inhibition works.

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 B, It partly depolarises the terminal, reducing spike amplitude and calcium entry. In presynaptic inhibition, GABA acting on terminals with high intracellular chloride depolarises them modestly.

Why is "It cleaves SNARE proteins and blocks vesicle fusion" not the answer?

Cleavage of SNARE proteins is the mechanism of botulinum and tetanus toxins.

Why is "It hyperpolarises the postsynaptic membrane through chloride entry" not the answer?

Hyperpolarising the postsynaptic membrane is postsynaptic inhibition.

Why is "It speeds reuptake of the transmitter from the cleft" not the answer?

Faster reuptake would shorten transmitter action but is not how axo-axonal inhibition works.

What concept does this question test?

It tests Nerve and muscle: presynaptic inhibition in Physiology. This inactivates some sodium channels, reduces the amplitude of the arriving spike and so the calcium entry that triggers release, while the postsynaptic cell itself is not hyperpolarised.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. 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: presynaptic inhibition?

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.