16 Action potential conduction

Learning Objectives

After reading this section, you should be able to-

  • Describe the importance of voltage-gated channels in the conduction (propagation) of an action potential.
  • Explain how axon diameter and myelination affect conduction velocity.
  • Explain the role of myelin in saltatory conduction.
  • Compare action potential conduction (propagation) in an unmyelinated versus a myelinated axon.

Propagation of the Action Potential

The action potential is initiated at the beginning of the axon, at what is called the initial segment, or the (trigger zone). Rapid depolarization can take place here due to a high density of voltage-gated Na+channels. Going down the length of the axon, the action potential is propagated because more voltage-gated Na+ channels are opened as the depolarization spreads. This spreading occurs because Na+ enters through the channel and moves along the inside of the cell membrane. As the Na+ moves, or flows, a short distance along the cell membrane, its positive charge depolarizes a little more of the cell membrane. As that depolarization spreads, new voltage-gated Na+ channels open and more ions rush into the cell, spreading the depolarization a farther.

Because voltage-gated Na+ channels are inactivated at the peak of the depolarization, they cannot be opened again for a brief time. This brief period of time when Na+ channels cannot be opened is called the (absolute refractory period). Because of this, positive ions spreading back toward previously opened channels has no effect on the membrane potential. Therefore, action potential must propagate from the trigger zone toward the axon terminals.

Propagation, as described above, applies to unmyelinated axons. When myelination is present, the action potential propagates differently, and the speed of signal conduction is optimized. In a myelinated axon, sodium ions that enter the cell at the trigger zone start to spread along the length of the axon segment, but there are no voltage-gated Na+ channels until the first node of Ranvier. Because there is not constant opening of these channels along the axon segment, the depolarization spreads at an optimal speed. The distance between nodes is the optimal distance to keep the membrane still depolarized above threshold at the next node. As Na+ spreads along the inside of the membrane of the axon segment, the charge starts to dissipate. If the node were any farther down the axon, that depolarization would fall off too much for voltage-gated Na+ channels to be activated at the next node of Ranvier. If the nodes were any closer together, the speed of propagation would be slower.

Propagation along an unmyelinated axon is referred to as continuous conduction; along the length of a myelinated axon, it is referred to as saltatory conduction. Continuous conduction is slow because there are always voltage-gated Na+ channels opening, and more and more Na+ is rushing into the cell. Saltatory conduction is faster because the action potential “jumps” from one node to the next (saltare = “to leap”), and the new influx of Na+ renews the depolarized membrane. Along with the myelination of the axon, the diameter of the axon can influence the speed of conduction. Much as water runs faster in a wide river than in a narrow creek, Na+-based depolarization spreads faster down a wide axon than down a narrow one. This concept is known as resistance and is generally true for electrical wires or plumbing, just as it is true for axons, although the specific conditions are different at the scales of electrons or ions versus water in a river.

Adapted from Anatomy & Physiology by Lindsay M. Biga et al, shared under a Creative Commons Attribution-ShareAlike 4.0 International License, chapter 12.

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