Propagation of the Action Potential
So far, we have considered the ion flow at just one point on the neuron’s membrane: When the membrane is perturbed at that location, the ion channels there open, sodium ions rush in, and the cell interior at that region briefly loses its negative charge. We said earlier, though, that the neuron doesn’t just respond to an input; it also transmits this response from one end of the neuron to other. Specifically, the neuron sends a signal down its axon, where it will eventually launch a new series of events triggering the next neuron. How does this transmission work?
As we’ve just noted, when a neuron’s membrane is disturbed, it is briefly depolarized— that is, it loses the electrical charge that normally exists across the membrane. This depolar-ization takes place at a particular location; but it spreads because depolarization at one point on the membrane causes other nearby ion channels to open, and so sodium rushes into the cell at those locations as well. Of course, the resting potential is quickly restored at those locations, but—for a brief moment—a new portion of the cell’s membrane has beendepolarized. This depolarization causes the next set of ion channels to open, which causes the next set to open, and so on in a domino-like sequence as the action potential at one site triggers an action potential at the next. In this way, the depolarization moves down the entire length of the axon and throughout the rest of the neuron as well. This sequence of events is known as the propagation of the action potential. The whole thing is like a spark traveling along a fuse—except that whereas the fuse is consumed by the spark, the ion channels rapidly reclose and the membrane restores itself (i.e., reestablishes the resting potential; Figure 3.11).
One might worry that this process could continue infinitely—as one region of the membrane depolarizes its neighbor, which in turn causes a new depolarization of the first region, which then depolarizes the neighbor again, and on and on. This back-and-forth disruption is prevented by the refractory period at each area of the mem-brane. Thanks to the refractory period, the area of membrane that was depolarized first is unresponsive when, a moment later, its neighbor is depolarized. As a result, the action potential is propagated in one direction only and thus works its way down the axon.
The flow of ions in or out of the neuron is, as we’ve said, quite rapid. Even so, the propagation of the action potential is surprisingly slow—it travels at about 1 meter per second, roughly the walking speed of an average adult. If this was top speed for neural signals, it would be disastrous for most organisms; fast-paced actions would be impossi-ble. This problem is solved, however, by an anatomical feature we’ve already mentioned: the myelin layers that wrap around an axon and—crucially—the gaps between the myelin wrappers.
If an axon is myelinated, ions can move into or out of the axon only at the nodes of Ranvier. At all other locations, the axon is enclosed within its myelin wrapper, and this blocks ion flow. In essence, therefore, the action potential has to skip from node to node; and thanks to these jumps, it moves relatively quickly: Myelinated axons can propagate their action potentials at speeds up to 120 meters per second (about 260 miles per hour).
To appreciate the huge importance of the myelin, consider the deficits someone suf-fers when myelination breaks down in the brain. This happens in multiple sclerosis(MS), a disease in which the body’s immune system mistakenly regards the myelin as an intruder and attacks it. The manifestations of MS are variable but severe, and they can include such serious maladies as total blindness and paralysis.
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