Saltatory Conduction: Why Myelin Makes Signals Fast

How action potentials 'jump' from one node of Ranvier to the next along myelinated axons — and why this lets vertebrates send fast signals through thin nerves.

Nerve signals need to be fast: a tall person's brain must control their toes over a metre away. There are two ways to speed up an axon. One is to make it wider — the squid's strategy, which is why its escape axons are up to about a millimetre thick. The other is to insulate it — the vertebrate strategy.

Jumping between nodes

Myelin wraps the axon in segments, leaving gaps about a micrometre wide — the nodes of Ranvier, named after the French anatomist Louis-Antoine Ranvier, who described them in 1878. Voltage-gated sodium channels are densely packed at the nodes and scarce beneath the myelin.

When a spike fires at one node, current flows inside the axon to the next node. Because myelin stops it leaking out through the membrane in between, enough current arrives to push the next node past threshold, which fires its own spike. The signal is regenerated only at nodes, so it appears to leap — saltare is Latin for "to jump". The Japanese physiologist Ichiji Tasaki demonstrated this experimentally in the late 1930s.

Faster, thinner, cheaper

The fastest myelinated axons conduct at about 100–120 metres per second. An unmyelinated axon of the same diameter might conduct at 1 metre per second. Myelin lets the human nervous system pack millions of fast fibres into narrow nerves; to match the speed without myelin, our spinal cord would have to be enormously thick. And because ions only cross the membrane at nodes, myelinated axons use far less energy per spike.

When the jumps fail

If myelin is damaged, as in multiple sclerosis, current leaks away between nodes. Signals slow down, become unreliable or fail to reach the next node at all, producing symptoms such as blurred vision, weakness and numbness. Heat makes things worse — many people with MS notice symptoms worsen in a hot bath.