The mechanism of electrotonic spread of depolarization can be observed in Fig. 5.8. It demonstrates how a current that enters through one part of the membrane can depolarize the neighboring membrane. A similar effect occurs when the Na+ channels are opened by an action potential at one site along the axon. However, in this case, the current is strong enough to depolarize the areas on either side past the threshold, resulting in the generation of action potentials in these neighboring areas. The inward Na+ current in these areas can then provide the current required to depolarize their neighbors past the threshold, leading to the generation of action potentials in those areas as well. This process repeats, allowing the action potential to propagate down the axon while maintaining the same size and shape.

Typically, action potentials originate at the axon's initial segment, which is attached to the neuron cell body or proximal dendrite, and then travel to the terminal end. This is because the initial segment has a higher density of voltage-gated Na+ channels, making it more prone to spiking than the soma or dendrites. However, axons are not limited to unidirectional conduction. As shown in Fig. 5.8, an action potential initiated by a depolarization in the middle of an axon is simultaneously conducted in both directions from the initiation site.

But why does a spike that starts at the initial segment not propagate in both directions? In reality, it does. Along with propagating down the axon, the current flowing from the initial segment back to the soma can also trigger a spike in the soma due to the presence of voltage-gated Na+ channels. However, additional "backpropagating" spikes from the axon do not occur, and the somatic spike does not cause the initial segment of the axon to fire a second time and start a repeating cycle. This is because the refractory period of the membrane prevents an area that has already spiked from firing a second spike for a brief period. Therefore, when a spike originating from the initial segment starts traveling down the axon, the depolarization of the membrane on both sides of the site occurs. However, the side closer to the cell body, which has recently fired a spike, is unable to respond to this depolarization due to the inactivation of its Na+ channels. By the time the Na+ channels become de-inactivated and ready to open, the depolarization at that site has ended since the action potential lasts for approximately 1 millisecond. Thus, the inactivation gate of the Na+ channel not only determines the duration of the action potential but also ensures its singular and unidirectional propagation from its origin at the initial segment.

The speed of conduction in a nerve fiber depends on the electrical properties of the cytoplasm and the plasma membrane surrounding the fiber, as well as its geometry. In nonmyelinated fibers, the conduction velocity is proportional to the square root of the cross-sectional diameter (Fig. 5.9). This relationship is influenced by the changes in ra (axial resistance) and rm (membrane resistance) with diameter. As the fiber diameter increases, ra decreases exponentially with the square of the diameter, while rm increases linearly with diameter. Consequently, the resistance to current decreases, resulting in faster conduction velocity.
Fig. 5.8 shows how in a local response the current that flows in through one part of the membrane acts to depolarize the neighboring membrane. The same thing happens when the Na+ channels are opened by an action potential at one site along the axon, except that in this case, the current will be large enough to depolarize the areas on either side past threshold and thus generate action potentials in these neighboring areas. The inward Na+ current in these areas can then provide the current to depolarize their neighbors past threshold so that they in turn generate action potentials, •Fig. 5.8 Mechanism of Electrotonic Spread of Depolarization. A, Thereversalofmembranepolaritythatoccurswithlocaldepolariza-tion.B, Thelocalcurrentsthatflowtodepolarizeadjacentareasofthemembraneandallowconductionofthedepolarization.B + – + – + – + – + – + – + – + – + – + – + – + – + – + – – + – + – + + – + – + – – + – + – + – + – + – + – + – + – + – + – + – + – + – + and so on. In short, action potential propagation along an axon involves recurring cycles of depolarization to provide sufficient local current flow for generation of an action potential in an adjacent region of the cell membrane. Thus the action potential is said to be propagated down the axon, with “new” action potentials being generated along its length. In this way, the action potential can propagate down the entire length of the axon while retaining the same size and shape.
Normally, action potentials are first generated at the axon’s initial segment (i.e., where the axon is attached to the neuron cell body or proximal dendrite) and then conducted to the terminal end. The reason for this is that the initial segment has a very high density of voltage-gated Na+ channels, and thus it has a lower threshold for spiking than does the soma or dendrites. However, axons are not inherently unidirectional conductors. For example, as implied by the local circuits shown in
Fig. 5.8 , an action potential generated by a depolarization in the middle of an axon is conducted in both directions from its initiation site simultaneously.
Why does a spike that starts at the initial segment not propagate in both directions? In fact, it does. In addition to propagating down the axon, the current flowing from the initial segment back to the soma can cause a spike to be generated in the soma because the soma also has voltage-gated Na+ channels. Additional “backpropagating” spikes from the axon do not occur, however, nor does the somatic spike cause the initial segment of the axon to fire a second time (and thereby send another spike down the axon and start a repeating cycle). This does not happen because the refractory period of the membrane makes any area that has already spiked unable to fire a second spike for a short time. Thus for a spike that started at the initial segment and has begun traveling down the axon, current flowing in at the site of the spike depolarizes the membrane on both sides of that site. However, the side closer to the cell body, which has recently fired a spike, cannot respond to this depolarization because its Na+ channels are still inactivated. By the time Na+ channels are de-inactivated (have returned to their closed state and would be able to open) the depolarization of membrane at that site has ended (because the action potential lasts only for ≈1 msec). Thus the inactivation gate of the Na+ channel not only helps determine the duration of the action potential but it also is responsible for its singular and unidirectional propagation from its origin at the initial segment.
The speed of conduction in a nerve fiber is determined by the electrical properties of the cytoplasm and the plasma membrane that surrounds the fiber, as well as by its geometry. In nonmyelinated fibers, conduction velocity is proportional to the square root of the cross-sectional diameter (Fig. 5.9 ). This effect is related to the changes in ra and rm with diameter. As the diameter of a fiber increases, ra decreases with the square of the diameter, and rm increases only linearly with diameter; as a result, resistance to current •Fig.