Questions: Action Potential Generation and Propagation

Question 1

During an action potential, what causes depolarization to spread to adjacent regions of the axon?

• A. Electrical current flows down the axon from the initial segment, like current through a wire
• B. Local circuit currents from the depolarized patch flow laterally to adjacent membrane, depolarizing it past threshold
• C. The sodium-potassium pump actively transports positive charge to neighboring membrane regions
• D. Voltage-gated channels open simultaneously along the entire axon length in response to the initial stimulus

Answer: (B)

The action potential is not a current flowing down the axon like water in a pipe — it is regenerated at each point. When one membrane patch depolarizes, positive charge flows laterally inside the axon to the adjacent resting membrane (local circuit currents). This small current depolarizes the neighboring patch past threshold, triggering its own Na⁺ channel cascade. The wave moves by sequential regeneration, not transmission. Option A is the classic misconception.

Question 2

A toxin permanently blocks voltage-gated Na⁺ channel inactivation — channels can open normally but cannot transition to the inactivated state. What is the most likely effect on a neuron exposed to this toxin?

• A. Neurons fire more rapidly, since more sodium influx means a stronger signal
• B. Action potentials propagate faster because Na⁺ channels remain open longer at each site
• C. The neuron becomes stuck in a prolonged depolarized state and cannot generate further action potentials
• D. Repolarization is faster because K⁺ channels overcompensate for the stuck Na⁺ channels

Answer: (C)

Na⁺ channel inactivation is what terminates the depolarizing phase and establishes the absolute refractory period. Without inactivation, Na⁺ channels remain open indefinitely, keeping the membrane depolarized near +40 mV. The neuron cannot repolarize, cannot re-activate its voltage-gated channels, and is locked in a state that prevents any subsequent action potential. This is the mechanism by which several neurotoxins (e.g., batrachotoxin) cause persistent depolarization and nerve failure.

Question 3

An action potential's amplitude decreases progressively as it travels further from the site of initiation, eventually fading out — similar to how a ripple in water weakens with distance.

• T. True
• F. False

Answer: False

This describes a decremental (graded) potential, not an action potential. The action potential is all-or-none and is regenerated de novo at each point along the axon by the opening of fresh voltage-gated Na⁺ channels. Each regeneration event produces a full-amplitude spike, so the signal maintains its size across the entire axon length. The refractory period behind the advancing wave prevents it from reversing direction, but amplitude does not decay with distance.

Question 4

The absolute refractory period — during which no stimulus can trigger another action potential — is what ensures that action potentials propagate in only one direction along an axon.

• T. True
• F. False

Answer: True

After a patch of membrane fires, its Na⁺ channels enter the inactivated state and remain so for 1–2 ms (the absolute refractory period). The region that just fired therefore cannot re-fire even if the advancing depolarization wave loops back to it. This means the depolarization can only trigger the next, not-yet-fired patch in the forward direction — enforcing unidirectional conduction. Without the refractory period, signals could travel in both directions or create re-entrant loops.

Question 5

Explain why myelin dramatically increases conduction velocity rather than simply allowing the action potential to decay, as passive electrical signals do.

Model answer: Myelin insulates the axon segments between nodes of Ranvier, dramatically reducing ion leakage and membrane capacitance along those segments. When an action potential fires at one node, the resulting local circuit current spreads with minimal attenuation along the myelinated internodal segment and reaches the next node of Ranvier with enough strength to depolarize it past threshold. The action potential effectively 'jumps' from node to node (saltatory conduction) rather than being regenerated at every point. Each saltatory jump covers far more distance per regeneration event than unmyelinated propagation, producing conduction velocities up to 100 m/s — compared to ~1 m/s in small unmyelinated fibers.

The key is that myelin does not just speed up propagation — it changes its mechanism from continuous to saltatory. In unmyelinated fibers, every patch of membrane must be depolarized past threshold to regenerate the signal, which is slow. In myelinated fibers, the insulation makes the internodal membrane electrically 'invisible,' so current jumps directly between nodes where the voltage-gated channels are concentrated. This is why demyelinating diseases (multiple sclerosis, Guillain-Barré) cause dramatic slowing or failure of conduction — they eliminate the saltatory mechanism.