2.3 Saltatory Conduction, Myelin, and Nodes of Ranvier

2.3 Saltatory Conduction, Myelin, and Nodes of Ranvier

Jumping is faster than crawling

Saltatory conduction (from Latin saltare, to leap) is propagation in which the action potential (AP) is regenerated at successive nodes of Ranvier and appears to jump from node to node rather than crawling continuously along every micrometer of membrane. Between nodes, myelin allows rapid passive spread of depolarizing current. At the node, a dense patch of voltage-gated Na+ channels fires a new AP.

Local-circuit current makes the jump concrete. When a node fires, Na+ enters and the interior of that node becomes positive. Current flows down the axoplasm to the next node, depolarizes it from the inside, and returns in the extracellular space. If the next node reaches threshold, it fires, and the process repeats. Myelin's job is to keep that internodal current from leaking out through the internodal membrane before it arrives.

This is the conduction mode of the large sensory and motor axons that dominate routine nerve conduction study (NCS) recordings. Sensory nerve action potentials (SNAPs) and compound muscle action potentials (CMAPs) are the extracellular volleys of those large fibers. Unmyelinated axons (C fibers) cannot saltate; they conduct continuously and slowly.

Who makes myelin: Schwann cells versus oligodendrocytes

In the peripheral nervous system (PNS) — spinal nerve roots distal to central myelin, plexuses, and peripheral nerves — Schwann cells produce compact myelin. A myelinating Schwann cell typically wraps one internodal segment of one PNS axon. That 1:1 internodal relationship matters when a Schwann cell is lost: one internode of one axon is denuded.

Schwann cells also invest unmyelinated axons, but without compact myelin. In a Remak bundle, one non-myelinating Schwann cell can ensheath several C fibers. So "Schwann cell" does not automatically mean "fast saltatory conduction." Compact myelin, internodes, and nodes are the saltatory kit; Remak investment is a different geometry.

In the central nervous system (CNS), oligodendrocytes myelinate axons, and one oligodendrocyte can wrap internodes on multiple axons. Candidates mix these cells constantly. For NCS you are stimulating PNS axons: think Schwann cells. CNS myelin disease is not what a routine median SNAP is testing, even though the saltatory mechanism is analogous.

Myelin is multilamellar lipid-rich membrane. Electrically it increases transmembrane resistance (less current leaks across the internodal membrane) and decreases membrane capacitance (less charge is needed to change internodal voltage). Both changes favor rapid, long-distance passive spread to the next node.

Anatomy of a node and an internode

The node of Ranvier is a bare axonal gap between Schwann-cell territories. It is packed with voltage-gated Na+ channels — orders of magnitude higher density than internodal membrane. Flanking paranodes and juxtaparanodes organize K+ channels and adhesion molecules; for this domain, remember that the node is the Na+ regeneration site and the internode is the insulated cable.

Internodal length scales with axon diameter in healthy nerve. Large fibers have longer internodes (on the order of 1 mm in big human fibers, with textbook ranges from several tenths of a millimeter up to about 1–2 mm). Longer internodes mean fewer regeneration sites per centimeter and faster conduction — provided current still arrives at the next node with a margin. If internodes are too long or myelin is too leaky, the next node may not reach threshold: that is the seed of conduction block, previewed here and developed in a later demyelination chapter.

After each nodal spike, Na+ has entered and some K+ has left. The sodium–potassium pump (Na+/K+ ATPase) restores those gradients so Nernst batteries do not run down. Because Na+ entry is concentrated at nodes, pumping is concentrated there too. That is a major energy advantage of saltatory design: you do not pay the full Na+ tax along every square micrometer of internodal membrane.

Length constant and time constant (conceptual)

Two passive cable numbers explain why myelin speeds conduction without requiring you to derive cable equations.

The length constant (λ, lambda) describes how far a local voltage change spreads along the fiber before decaying. High internodal membrane resistance (myelin) and low axial resistance (large axon diameter) increase λ. A larger λ means depolarizing current from one node still meaningfully depolarizes the next node.

The time constant (τ, tau) describes how quickly membrane voltage can change. It depends on resistance and capacitance. Myelin lowers effective capacitance, shortening τ, so nodal and internodal membrane charge toward threshold faster.

Together: myelin makes the internodal cable leak less and charge faster. Unmyelinated membrane leaks and is slow to charge, so the AP must be generated continuously along the axon, which is metabolically expensive and slow. Diameter still matters in both systems: a larger axon has lower axial resistance, so current spreads farther, which is why big fibers are fast even among myelinated populations.

A useful teaching rule of thumb is that myelinated conduction velocity in meters per second is roughly several times the axon diameter in micrometers (often taught near 6× for large fibers, as an order-of-magnitude memory aid, not a patient-specific calculator). Unmyelinated C-fiber velocity stays near 0.5–2 m/s regardless of how much gain you add on the NCS machine.

Myelinated versus unmyelinated axons

Safety factor is the ratio of current delivered to the next node versus current needed to reach threshold. Healthy myelinated fibers have a comfortable surplus, often taught as about 5:1 or greater. Thin the myelin, widen the node, or lengthen the leaky stretch, and safety factor falls. Slowing appears first (it takes longer to charge the next node). If current never reaches threshold, the AP dies: conduction block.

Degree of myelination tracks velocity. Heavily myelinated large fibers are the fastest. Thinly myelinated Aδ fibers (sharp pain, cold) conduct more slowly. Unmyelinated C fibers (slow pain, warmth, many postganglionic autonomic axons) are slowest. Aα motor axons to extrafusal muscle and large cutaneous/proprioceptive Aβ sensory axons are the populations whose saltatory volleys you mark for onset latency.

Why demyelination slows — and can block (preview)

Strip internodal myelin or disrupt paranodal seals and two cable disasters follow. Current leaks through the denuded internodal membrane (length constant falls). Capacitance of the exposed membrane rises (time constant lengthens). The next node charges more slowly: latency prolongs, velocity falls. If leak is severe, the node never reaches threshold: block. Partial block or temporal dispersion also reduces SNAP/CMAP amplitude and stretches duration because surviving impulses arrive out of synchrony.

This preview matters so you do not treat a slow velocity as "the axon is tired" or "the pump is weak" as a first explanation. Geometry and leak changed the cable. Pump failure can impair excitability too, but demyelinating slowing is primarily a myelin/node current-sharing problem. Remyelination, when it occurs, often produces shorter internodes (more Schwann cells crowding a formerly long internode). Velocity may improve but not always to the original value. That reconstruction story belongs in a later chapter; the candidate skill now is: myelin exists to raise safety factor and speed by saltatory current jump; lose myelin and the jump becomes a stumble or a fall.

Temperature belongs in the same physiologic chain. Cooling slows channel kinetics and conduction velocity; laboratories standardize limb temperature because myelin and nodal channels are temperature-sensitive. Velocity is never a pure anatomy number independent of the recording conditions.

What routine NCS is actually sampling

Supramaximal stimulation of a mixed or motor nerve preferentially activates large myelinated axons: α motor axons to extrafusal muscle and large cutaneous/proprioceptive sensory axons. Those fibers saltate, arrive nearly together, and produce sharp onset latencies. Onset latency and conduction velocity therefore describe the fastest remaining large fibers, not the average of every axon in the nerve and not the C-fiber pain population.

Small pain fibers are not hidden SNAPs waiting for more amplifier gain. They are a different population with different conduction physics. A patient can have severe small-fiber pain and a normal routine NCS. Conversely, a slow median sensory velocity is a large-fiber myelinated problem (or a technical error such as distance or temperature), not a C-fiber readout. If the clinical question is small-fiber neuropathy, routine NCS is the wrong tool even when you understand nodes of Ranvier perfectly.

OpenExamPrep laboratory translation: place the cathode, recruit large myelinated axons, and record a volley whose velocity reflects internodal saltatory conduction. Schwann cells, not oligodendrocytes, built that peripheral myelin. Nodes regenerate the spike. Pumps recharge the gradients at those nodes. Demyelination attacks this architecture; axonal loss removes the cables entirely.