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Myelinated axons achieve conduction velocities 50–100 times faster than unmyelinated axons through saltatory conduction: action potentials regenerate at nodes of Ranvier where ion channels are clustered, while insulating myelin prevents current leakage along internodes. This arrangement provides both rapid signaling and energy efficiency.
From your study of action potential repolarization, you understand how voltage-gated sodium and potassium channels generate a self-regenerating electrical signal that propagates along an axon. In an unmyelinated axon, this propagation is continuous: each patch of membrane depolarizes the next, and the action potential moves forward like a lit fuse. It works, but it is slow — roughly 0.5 to 2 meters per second in thin unmyelinated fibers. Saltatory conduction is evolution's solution for speed, and it depends on wrapping the axon in an insulating sheath of myelin.
Myelin is produced by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. These glial cells wrap their plasma membranes around the axon in tight, concentric layers — sometimes 50 to 100 wraps thick — creating a fatty insulating barrier. This insulation has two critical electrical effects. First, it dramatically increases the membrane resistance of the internode (the myelinated segment), meaning ions cannot easily leak out across the membrane. Second, it decreases the membrane capacitance, meaning less charge is needed to change the voltage. Together, these properties allow the local current generated by an action potential at one node to spread passively through the myelinated internode with very little loss — like sending current through a well-insulated wire instead of a leaky garden hose.
The action potential does not actually travel through the myelinated segments. Instead, it "jumps" from one node of Ranvier to the next. Nodes are short (~1 μm) gaps between myelin segments where the axon membrane is exposed and densely packed with voltage-gated sodium channels. When passive current from the previous node reaches a new node, it depolarizes the membrane to threshold, and a fresh action potential fires. The signal then spreads passively to the next node, where it regenerates again. This jumping pattern — from the Latin *saltare*, meaning "to leap" — is why the process is called saltatory conduction. Conduction velocity in myelinated fibers reaches 80 to 120 meters per second, fast enough that a signal from your toe reaches your brain in about 20 milliseconds.
Saltatory conduction also confers a major energy advantage. Because ion flux (and therefore ATP-dependent Na⁺/K⁺-ATPase pumping to restore gradients) only occurs at the nodes — which make up less than 1% of the axon's surface area — the metabolic cost of signaling is far lower than in continuous conduction. This matters enormously in the brain, which already consumes about 20% of the body's energy. The clinical consequence of myelin loss is devastating: in diseases like multiple sclerosis, autoimmune demyelination exposes internodal membrane that lacks sufficient ion channels, causing conduction block or severe slowing. Symptoms — vision loss, weakness, numbness — directly reflect which axonal tracts have lost their myelin insulation.