Saltatory Conduction
Saltatory conduction refers to the rapid propagation of action potentials along the myelinated axons of neurons. Myelinated axons are coated in a fatty substance called myelin, forming an insulating sheath (the myelin sheath) produced by oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS). The gaps in the myelin sheath are referred to as myelin sheath gaps, commonly referred to as nodes of Ranvier.
Unlike continuous conduction in nonmyelinated axons, where the electrical waveform travels down the entire length of the axon, saltatory conduction involves the 'leaping' of electric signals between successive myelin sheath gaps, skipping the myelinated regions in between. This transmission pattern speeds up the transmission of action potentials.
Definition | Rapid propagation of action potentials along myelinated axons in a “leaping” pattern between myelin sheath gaps |
Mechanism | Suprathreshold stimulus; Opening of voltage-gated Na+ channels at the axon hillock; Action potential initiation; Passive spread of depolarization underneath the myelin sheath; Regenerative depolarization once reaching a myelin sheath gap; “Leaping” transmission from gap/node to gap/node until the synaptic terminal. |
Advantages | Increased velocity; Energy conservation; Signal strength preservation |
Mechanism
When a neuron receives a suprathreshold stimulus, the voltage-gated Na+ channels at the axon hillock open, therefore allowing the influx of sodium ions for the initiation of an action potential. The initial action potential then causes depolarization in the adjacent region of the axonal membrane.
Myelinated axons exhibit a highly structured distribution of voltage-gated ion channels, with Na+ channels profoundly concentrated at the myelin sheath gaps (nodes of Ranvier). The myelin sheath effectively prevents the leakage of ions across the membrane, and the depolarization spreads passively along the axon underneath the myelin sheath until reaching a myelin sheath gap. There, it is regenerated by the voltage-gated Na+ channels. By this process of regenerative depolarization, the action potential 'leaps' from gap to gap, until it reaches the axon terminal. This whole process is called saltatory conduction and it plays an important role in the rapid propagation of action potentials in the nervous system.
Advantages
As described, saltatory action potential propagation in myelinated neurons is faster than the continuous propagation in nonmyelinated neurons of the same diameter, as it bypasses the myelinated areas. Additionally, saltatory conduction is metabolically efficient; depolarization passively spreads underneath the myelin sheath and actively regenerates at the nodes of Ranvier, thus requiring less energy compared to continuous conduction, where every segment of the axon undergoes active depolarization. Preservation of the signal strength is achieved via the insulating properties of the myelin sheath, preventing ion 'leakage' across the neuron and ensuring the reliable long-distance transmission of impulses.
Clinical notes
Guillain-Barré Syndrome (GBS) is a rare, immune-mediated neurological disorder that usually manifests as an acute inflammatory polyradiculoneuropathy, i.e. inflammation and damage to multiple nerve roots (polyradiculopathy) and peripheral nerves (polyneuropathy), with progressive motor weakness and diminished reflexes. While the exact cause is not fully understood, GBS often precedes an infection (e.g. Campylobacter jejuni, Cytomegalovirus, COVID-19).
In GBS, the immune system mistakenly attacks the peripheral nerves, leading to inflammation and damage of the myelin sheath. The most widely recognized form of GBS is acute inflammatory demyelinating polyradiculoneuropathy (AIDP) involving destruction of the myelin sheath by white blood cells, preceded by activation of the complement. As a result, saltatory action potential propagation is impaired, disrupting the normal neuronal function. Therefore, the transmission of nerve impulses becomes slower and less efficient
Clinical findings include numbness, tingling and/or pain, followed by bilateral progressive weakness of the limbs, with simultaneous areflexia, i.e. absence or significant decrease in the deep tendon reflexes, and dysautonomia, i.e. dysfunction of the autonomic nervous system (ANS).
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