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Physiology · Nerve and muscle: potassium channels in demyelinated axons
Sample itemIn multiple sclerosis, fampridine (4-aminopyridine) can improve walking speed. Which action explains the benefit?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. It blocks potassium channels exposed in demyelinated axons, restoring action potential conduction
When myelin is lost, voltage-gated potassium channels normally hidden under the sheath become exposed and leak current, which can block conduction. Blocking them prolongs the action potential and helps it reach the next node, improving conduction in surviving demyelinated axons.
Option by option
A. It blocks potassium channels exposed in demyelinated axons, restoring action potential conduction (correct)
Correct. Blocking exposed potassium channels restores conduction.
B. It stimulates remyelination by oligodendrocytes
It does not remyelinate; it improves conduction in axons that remain demyelinated.
C. It blocks NMDA receptors on motor neurones
NMDA receptor blockade is not its mechanism.
D. It opens sodium channels at the nodes of Ranvier
Fampridine does not open sodium channels; it blocks potassium channels.
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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