In vertebrate nervous systems, increasing the speed of APs by increasing the diameter of axons is not feasible because of the huge number of axons involved. Each of our eyes, for example, has about a million axons connecting it to the brain. These axons conduct APs at about the same speed as does the squid giant axon—about 20 meters per second—yet the diameter of each is 200 times smaller than the squid axon’s diameter. Imagine having optic tracts 200 times bigger. A different way of increasing conduction velocity of axons has evolved in vertebrates, and that adaptation is myelination.

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When glia wrap around axons, they cover the axons with concentric layers of myelin (see Figure 44.3). However, they leave regularly spaced gaps called nodes of Ranvier, where the axon is not covered (see Figure 44.10). Underneath the myelin sheaths, there are no Na⁺ or K⁺ channels, therefore, APs cannot propagate under the myelin sheath. However, an AP firing at a node of Ranvier creates a local electrical field inside the axon that spreads almost instantaneously to the next node of Ranvier. The resulting depolarization of that node triggers another AP, and so on down the axon. Thus the APs appear to jump from node to node, and their conduction down the axon is very fast.

The speed of conduction is increased in these myelin-wrapped axons because electric current flows much faster through the cytoplasm than ion channels can open and close. This form of rapid impulse propagation is called saltatory conduction (Latin saltare, “to jump”).