154
Chapter 6
Subthreshold
stimuli
Stimulus strength
Time
Threshold
stimulus
Threshold
potential
Resting
potential
0
+30
Membrane potential (mV)
Action potential
Subthreshold
potentials
–70
0
Figure 6–21
Changes in the membrane potential with increasing strength
of depolarizing stimulus. When the membrane potential
reaches threshold, action potentials are generated. Increasing
the stimulus strength above threshold level does not cause
larger action potentials. (The afterhyperpolarization has been
omitted from this fi gure for clarity, and the absolute value of
threshold is not indicated because it varies from cell to cell.)
as those caused by threshold stimuli. This is because once
threshold is reached, membrane events are no longer depen-
dent upon stimulus strength. Rather, the depolarization gen-
erates an action potential because the positive feedback cycle is
operating. Action potentials either occur or they do not occur
at all. Another way of saying this is that action potentials are
all-or-none.
The fi ring of a gun is a mechanical analogy that shows
the principle of all-or-none behavior. The magnitude of the
explosion and the velocity at which the bullet leaves the gun
do not depend on how hard the trigger is squeezed. Either the
trigger is pulled hard enough to fi
re the gun, or it is not; the
gun cannot be fi red halfway.
Because of its all-or-none nature, a single action potential
cannot convey information about the magnitude of the stimu-
lus that initiated it. How then do you distinguish between a
loud noise and a whisper, a light touch and a pinch? This infor-
mation, as we will discuss later, depends upon the number and
patterns of action potentials transmitted per unit of time (i.e.,
their frequency) and not upon their magnitude.
The generation of action potentials is prevented by
local
anesthetics
such as procaine
(
Novocaine
®
)
and lidocaine
Depolarization
of membrane
potential
Increased flow
of Na
+
into
the cell
Opening of
voltage-gated
Na
+
channels
Depolarizing
stimulus
Inactivation
of Na
+
channels
Increased P
Na
Start
Stop
Positive
feedback
Repolarization
of membrane
potential
Increased flow
of K
+
out of
the cell
Opening of
voltage-gated
K
+
channels
Depolarization
of membrane
by Na
+
influx
Increased P
K
Start
Negative
feedback
(a)
(b)
+
Figure 6–20
Feedback control in voltage-gated ion channels. (a) Sodium channels
exert positive feedback on membrane potential. (b) Potassium
channels exert negative feedback.
(
Xylocaine
®
)
because these drugs block voltage-gated sodium
channels, preventing them from opening in response to depo-
larization. Without action potentials, graded signals generated
in the periphery—in response to injury, for example—cannot
reach the brain and give rise to the sensation of pain.
Some animals produce toxins that work by interfering
with nerve conduction in the same way that local anesthet-
ics do. For example, the ovary of the puffer fi sh produces an
extremely potent toxin,
tetrodotoxin,
that binds to voltage-
gated sodium channels and prevents the sodium component of
the action potential. In Japan, chefs who prepare this delicacy
are specially trained to completely remove the ovaries before
serving the puffer fi sh dish called fugu. Individuals who eat
improperly prepared fugu may die, even if they ingest only a
tiny quantity of tetrodotoxin.
Refractory Periods
During the action potential, a second stimulus, no matter how
strong, will not produce a second action potential. That region
of the membrane is then said to be in its
absolute refractory
period.
This occurs during the period when the voltage-gated
sodium channels are either already open or have proceeded to
the inactivated state during the fi rst action potential. The inac-
tivation gate that has blocked these channels must be removed
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