Neuronal Signaling and the Structure of the Nervous System
155
by repolarizing the membrane and closing the pore before the
channels can reopen to the second stimulus.
Following the absolute refractory period, there is an
interval during which a second action potential can be pro-
duced, but only if the stimulus strength is considerably greater
than usual. This is the
relative refractory period,
which
can last 1 to 15 ms or longer and coincides roughly with the
period of afterhyperpolarization. During the relative refractory
period, some but not all of the voltage-gated sodium channels
have returned to a resting state, and some of the potassium
channels that repolarized the membrane are still open. From
this relative refractory state it is possible for a new stimulus to
depolarize the membrane above the threshold potential, but
only if the stimulus is large in magnitude or outlasts the rela-
tive refractory period.
The refractory periods limit the number of action poten-
tials an excitable membrane can produce in a given period of
time. Most nerve cells respond at frequencies of up to 100 action
potentials per second, and some may produce much higher fre-
quencies for brief periods. Refractory periods contribute to the
separation of these action potentials so that individual electrical
signals pass down the axon. The refractory periods also are key
in determining the direction of action potential propagation, as
we will discuss in the following section.
Action Potential Propagation
The action potential can only travel the length of a neuron if
each point along the membrane is depolarized to its threshold
potential as the action potential moves down the axon (
Figure
6–22
). As with graded potentials (refer back to Figure 6–15a),
the membrane is depolarized at each point along the way with
respect to the adjacent portions of the membrane, which are still
at the resting membrane potential. The difference between the
potentials causes ions to fl ow, and this local current depolar-
izes the adjacent membrane where it causes the voltage-gated
sodium channels located there to open. The current entering
during an action potential is suffi cient to easily depolarize the
adjacent membrane to the threshold potential.
The new action potential produces local currents of its
own that depolarize the region adjacent to it (
Figure 6–22b
),
producing yet another action potential at the next site, and so
on, to cause
action potential propagation
along the length
of the membrane. Thus, there is a sequential opening and clos-
ing of sodium and potassium channels along the membrane.
It is like lighting a trail of gunpowder—the action potential
doesn’t move, but it “sets off” a new action potential in the
region of the axon just ahead of it. Because each action poten-
tial depends on the positive feedback cycle of a new group of
sodium channels where the action potential is occurring, the
action potential arriving at the end of the membrane is virtu-
ally identical in form to the initial one. Thus, action potentials
are not conducted decrementally as are graded potentials.
Because a membrane area that has just undergone an
action potential is refractory and cannot immediately undergo
another, the only direction of action potential propagation is
away from a region of membrane that has recently been active.
If the membrane through which the action potential
must travel is not refractory, excitable membranes can con-
duct action potentials in either direction, with the direction of
propagation determined by the stimulus location. For exam-
ple, the action potentials in skeletal muscle cells are initiated
near the middle of the cells and propagate toward the two
ends. In most nerve cells, however, action potentials are initi-
ated at one end of the cell and propagate toward the other end
as shown in Figure 6–22. The propagation ceases when the
action potential reaches the end of an axon.
The velocity with which an action potential propagates
along a membrane depends upon fi ber diameter and whether
or not the fi ber is myelinated. The larger the fi ber diameter,
the faster the action potential propagates. This is because a
large fi ber offers less resistance to local current; more ions will
fl ow in a given time, bringing adjacent regions of the mem-
brane to threshold faster.
Myelin is an insulator that makes it more diffi cult for
charge to fl ow between intracellular and extracellular fl
uid
compartments. Because there is less “leakage” of charge across
the myelin, a local current can spread farther along an axon.
Moreover, the concentration of voltage-gated sodium chan-
nels in the myelinated region of axons is low. Therefore, action
potentials occur only at the nodes of Ranvier, where the myelin
coating is interrupted and the concentration of voltage-gated
sodium channels is high (
Figure 6–23
). Thus, action poten-
tials jump from one node to the next as they propagate along a
myelinated fi ber, and for this reason such propagation is called
saltatory conduction
(Latin,
saltare,
to leap).
Propagation via saltatory conduction is faster than
propagation in nonmyelinated fi bers of the same axon diam-
eter because less charge leaks out through the myelin-cov-
ered sections of the membrane. More charge arrives at the
node adjacent to the active node, and an action potential
is generated there sooner than if the myelin were not pres-
ent. Moreover, because ions cross the membrane only at the
nodes of Ranvier, the membrane pumps need to restore fewer
ions. Myelinated axons are therefore metabolically more
effi cient than unmyelinated ones. Thus, myelin adds speed,
reduces metabolic cost, and saves room in the nervous system
because the axons can be thinner. The loss of myelin at one
or several places in the nervous system occurs in the disease
multiple sclerosis.
This slows or blocks the propagation of
impulses, which results in poor coordination, lack of sensa-
tion, and partial paralysis (see Additional Clinical Examples
at the end of this section).
Conduction velocities range from about 0.5 m/s
(1 mi/h) for small-diameter, unmyelinated fi bers to about
100 m/s (225 mi/h) for large-diameter, myelinated fi
bers.
At 0.5 m/s, an action potential would travel the distance
from the toe to the brain of an average-sized person in about
4 s; at a velocity of 100 m/s, it takes about 0.02 s. Perhaps
you’ve dropped a heavy object on your toe and noticed that
an immediate, sharp pain (carried by large-diameter, myelin-
ated neurons) occurs well before the onset of a dull, throbbing
ache (transmitted along small, unmyelinated neurons).
Generation of Action Potentials
In our description of action potentials thus far, we have spo-
ken of “stimuli” as the initiators of action potentials. These
stimuli bring the membrane to the threshold potential, and
voltage-gated sodium channels trigger the all-or-none action
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