Immediately after blocking: the axon still conducts. The concentration gradients — high K⁺ and low Na⁺ inside, low K⁺ and high Na⁺ outside — are already established, and a single impulse moves only a very small number of ions. So a stimulus will still make the membrane freely permeable to Na⁺ at that site, Na⁺ will rush in, polarity will reverse and an action potential will be generated and conducted normally.

After a long interval: conduction fails. The ionic gradients across the resting membrane are maintained by the active transport of ions by the sodium-potassium pump, which transports 3 Na⁺ outwards for 2 K⁺ into the cell. With the pump blocked, every impulse and every leak runs the gradients down and nothing restores them. Once the concentration difference is gone, an opening of sodium channels produces no inward rush, no depolarisation and therefore no nerve impulse.

The principle: the pump does not create the impulse — it maintains the stored gradient that the impulse spends. Like a battery, it must be recharged between uses.

Permeability. At rest, the axonal membrane is comparatively more permeable to K⁺ and nearly impermeable to Na⁺. Since K⁺ is at high concentration inside, it tends to diffuse outwards down its gradient, carrying positive charge out of the cell. Sodium cannot come in to replace that charge, because the membrane is nearly impermeable to it. In addition, the membrane is impermeable to the negatively charged proteins present in the axoplasm, so those negative charges are trapped inside and cannot follow the potassium out.

Stoichiometry. The pump transports 3 Na⁺ outwards for 2 K⁺ into the cell. That is three positive charges out for every two in — a net loss of one positive charge from the interior per cycle. So the pump's own action also makes the outside more positive, despite carrying potassium inwards.

Together: outward leak of K⁺, trapped internal anions, and a pump with an unequal ratio all push in the same direction. The outer surface of the axonal membrane possesses a positive charge while its inner surface becomes negatively charged — the membrane is polarised.

In a wire the original signal itself travels the whole distance and is progressively lost to resistance, so it arrives weakened.

In an axon the signal is regenerated afresh at every point. The action potential at site A causes current to flow on the inner surface from A to B and on the outer surface from B to A, completing the circuit. This reverses the polarity at B, so a new action potential is generated at site B. That new action potential has the same magnitude as the one at A, because its size is set by the ion gradients and permeability of the membrane at B — not by how strong the signal at A was.

Since the sequence is repeated along the length of the axon, each point produces a full-sized impulse. Nothing is being carried and attenuated; the impulse is rebuilt at every step, which is why distance does not weaken it.

Why it must be brief. The rise in permeability to Na⁺ is quickly followed by a rise in permeability to K⁺, and within a fraction of a second K⁺ diffuses outside the membrane and restores the resting potential at the site of excitation. Only then does the fibre become once more responsive to further stimulation. A neuron that could not recover could not carry a second impulse.

If sodium permeability stayed high: Na⁺ would continue to enter and the site would remain depolarised, with the inner surface positive. The resting potential would never be restored. Three consequences follow:

(i) the neuron could not fire again, since there is no polarised state left to reverse — it would be permanently refractory at that site;

(ii) information could no longer be encoded, because a nervous system conveys intensity and duration through repeated impulses, which requires repeated recovery;

(iii) the ionic gradients would run down as sodium equilibrated across the membrane, and the sodium-potassium pump would be unable to keep pace.

An action potential can be generated only where ions can cross the membrane — that is, where the membrane can become freely permeable to Na⁺ and allow the rapid influx that reverses polarity.

Non-myelinated axon: the axon is enclosed by a Schwann cell that does not form a myelin sheath, so the membrane is available along its whole length. The sequence of depolarisation must therefore be repeated at every successive point, step by step, all the way along.

Myelinated axon: the axon is enveloped with Schwann cells forming a myelin sheath, and the membrane is exposed only at the nodes of Ranvier — the gaps between two adjacent myelin sheaths. The local current generated at one node therefore reaches the next node and regenerates the action potential there, effectively skipping the insulated stretches in between.

Conclusion: the myelinated axon needs far fewer regeneration events to cover the same distance, so it conducts faster. This is consistent with myelinated nerve fibres being found in the spinal and cranial nerves, where impulses must travel long distances quickly.