Myelination & Saltatory Conduction

Picture passing a bucket of water down a line of people. Hand-to-hand all the way down is slow. But if a few strong people stand far apart and toss the bucket between them, it races down the line. A myelinated nerve fibre works like the second line: the electrical signal effectively jumps from gap to gap instead of crawling along every patch of membrane. That speed is why your hand can leave a hot stove before you consciously feel the burn.

Myelin is a fatty insulating wrap — built by Schwann cells in the body and oligodendrocytes in the brain — coiled around the axon. It leaves bare gaps, the nodes of Ranvier (about 1 mm apart), each crammed with sodium channels. The action potential is only rebuilt at the nodes; under each insulated stretch the current spreads quickly and passively to the next node. This leaping is called saltatory conduction (Latin saltare, to leap). A handy rule of thumb is $v \approx 6d$, where $d$ is the outer fibre diameter in micrometres and $v$ is the speed in metres per second. A 10 μm fibre gives $v \approx 6 \times 10 = 60$ m/s.

The key quantity is the cable length constant $\lambda = \sqrt{R_m\,d/(4R_a)}$ — how far a passive voltage signal travels before it fades. Wrapping the axon about 150 times multiplies the membrane resistance $R_m$ and shrinks the membrane capacitance $C_m$, so $\lambda$ grows roughly tenfold and far less charge $Q = C_m V$ is needed to depolarise the next stretch. Once $\lambda$ exceeds the node spacing, one node's spike easily drives the next past threshold. Bare axons lack this trick, so their speed only creeps up as $v \propto \sqrt{d}$. In multiple sclerosis, myelin is stripped away, $\lambda$ collapses below the node spacing, and the signal can die between nodes — a conduction block.

Press Play and step through the presets to compare regimes. Push the parameter sliders toward the well-myelinated extreme and watch how readily the signal carries; then drop them toward the demyelinated extreme to see conduction falter — the same failure that underlies MS symptoms. Finally, raise the input slider and notice how a stronger drive can rescue a marginal fibre, a hint of why temperature shifts (the Uhthoff phenomenon) can swing symptoms either way.

Schwann cells (PNS)/oligodendrocytes (CNS) wrap axon ~150 times. R_m,myelin = 150×R_m ≈ 3×10⁶ Ω·cm². C_m,myelin = C_m/150 ≈ 0.007 μF/cm². λ_myelin = 10× λ_bare. Charge needed to depolarise: Q = C_m V → 150× less charge needed per unit length.

Nodes of Ranvier (1 μm wide, 1 mm spacing): 1000 Na⁺ channels/μm². AP at one node → current flows passively to next node (λ >> 1 mm). Depolarises next node above threshold → new AP. Jump time ≈ 0.05 ms → v ≈ 1 mm/0.05 ms = 20 m/s. 10 μm myelinated: 60 m/s vs 0.5 m/s unmyelinated.

Autoimmune myelin destruction: R_m drops 100×, C_m increases 100×, λ decreases 10×. AP from one node cannot reach next (λ < node spacing) → conduction block. Uhthoff phenomenon: symptoms worsen with fever (Na⁺ kinetics faster at high T → shorter AP → conduction block more likely). Treatment: 4-aminopyridine (K⁺ blocker) prolongs AP duration.