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saltatory conduction

Physiology / NeuroscienceNervous system (central)Nervous system (peripheral)

Summary

Saltatory conduction is the "jumping" propagation of action potentials between nodes of Ranvier along myelinated axons. Myelin increases membrane resistance and decreases capacitance, so depolarization spreads passively and rapidly between nodes, where voltage-gated Na+ channels regenerate the signal. This increases conduction velocity and energy efficiency, and its disruption causes demyelinating diseases (MS, GBS).

Detail

**Mechanism** - Myelin (oligodendrocytes in CNS; Schwann cells in PNS) wraps axons in insulating layers, raising membrane resistance and lowering capacitance. - Voltage-gated Na+ channels are densely clustered at the nodes of Ranvier (unmyelinated gaps), with K+ channels concentrated in the juxtaparanodal region. - An action potential at one node causes local current flow through the axoplasm (passive, electrotonic spread) under the myelin to the next node. The current depolarizes that node to threshold, regenerating the action potential. The signal appears to "jump" from node to node.

**Determinants of conduction velocity** - Velocity increases with myelination and with larger axon diameter (lower internal resistance). This is the length constant (λ) principle: λ = √(r_m/r_i). - Myelin raises r_m and lowers capacitance, so λ increases and less charge is needed to depolarize the next node. - Examples: A-alpha fibers (large, heavily myelinated) conduct fastest, around 80–120 m/s. C fibers (unmyelinated, small) conduct slowest, around 1 m/s.

**Advantages** - Faster conduction without needing giant axons (the squid giant axon is the unmyelinated alternative). - Energy efficiency: ion flux (and thus Na+/K+-ATPase work) is limited to the nodes.

**Clinical correlations (high-yield)** - **Multiple sclerosis**: CNS demyelination (autoimmune, T-cell mediated, oligodendrocyte loss). It causes conduction slowing or block, with internuclear ophthalmoplegia, optic neuritis, and spastic weakness. Oligoclonal bands in CSF, periventricular plaques on MRI. - **Guillain-Barré syndrome**: PNS demyelination (Schwann cells) after infection (e.g., Campylobacter jejuni). Ascending paralysis, areflexia, albuminocytologic dissociation in CSF. - **CIDP**: chronic PNS demyelination. - **Progressive multifocal leukoencephalopathy (PML)**: JC virus infects oligodendrocytes in immunosuppressed patients. - **Central pontine myelinolysis (osmotic demyelination)**: overly rapid correction of hyponatremia. - **Charcot-Marie-Tooth**: hereditary demyelinating neuropathy (PMP22 duplication in CMT1A). - **Metachromatic leukodystrophy, Krabbe disease**: lysosomal storage diseases that impair myelin. - **Local anesthetics** (e.g., lidocaine) block voltage-gated Na+ channels. Small, myelinated, rapidly firing fibers are blocked first.

**Key pearls** - Myelin differences: one oligodendrocyte myelinates multiple CNS axons, while one Schwann cell myelinates a single PNS axon segment. - Nerve conduction studies in demyelination show decreased conduction velocity and prolonged distal latency. Axonal loss instead shows decreased amplitude. - Conduction block occurs when demyelination is so severe that the current cannot reach threshold at the next node. - Temperature sensitivity in MS (Uhthoff phenomenon): symptoms worsen with heat because Na+ channel inactivation speeds up and conduction in demyelinated fibers fails.

Sources

  • First Aid for the USMLE Step 1 (Neurology/Neuroscience and Physiology sections)
  • Costanzo Physiology (Autonomic and nerve physiology, action potential propagation)
  • Guyton and Hall Textbook of Medical Physiology (Membrane potentials and action potentials)
  • Kandel's Principles of Neural Science (Propagation of the action potential)
  • Pathoma / Robbins Basic Pathology (Demyelinating disorders)

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.