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Physiology · Nerve and muscle: presynaptic inhibition
Sample itemIn 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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