Neuronal Signaling and the Structure of the Nervous System
153
You might think that large movements of ions across
the membrane are required to produce such large changes in
membrane potential. Actually, the number of ions that cross
the membrane during an action potential is extremely small
compared to the total number of ions in the cell, producing
only infi nitesimal changes in the intracellular ion concentra-
tions. Yet, if this tiny number of additional ions crossing the
membrane with repeated action potentials were not eventually
moved back across the membrane, the concentration gradi-
ents of sodium and potassium would gradually dissipate, and
action potentials could no longer be generated. As might be
expected, cellular accumulation of sodium and loss of potas-
sium are prevented by the continuous action of the membrane
Na
+
/K
+
-ATPase pumps.
As explained previously, not all membrane depolariza-
tions in excitable cells trigger the positive feedback relation-
ship that leads to an action potential. Action potentials occur
only when the initial stimulus plus the current through the
sodium channels it opens are suffi cient to elevate the mem-
brane potential beyond the threshold potential. Stimuli that
are just strong enough to depolarize the membrane to this
level are
threshold stimuli
(
Figure 6–21
). The threshold of
most excitable membranes is about 15 mV less negative than
the resting membrane potential. Thus, if the resting potential
of a neuron is –70 mV, the threshold potential may be –55 mV.
At depolarizations less than threshold, the positive feedback
cycle cannot get started. In such cases, the membrane will
return to its resting level as soon as the stimulus is removed,
and no action potential will be generated. These weak depo-
larizations are
subthreshold potentials,
and the stimuli
that cause them are
subthreshold stimuli.
Stimuli of
more than
threshold magnitude elicit action
potentials, but as can be seen in Figure 6–21, the action poten-
tials resulting from such stimuli have exactly the same amplitude
P
K
P
Na
Na
+
K
+
Membrane potential (mV)
Time (ms)
Relative membrane permeability
(a)
(b)
+30
0
–70
600
300
100
01
2
3
4
3
2
4
5
6
7
1
1
K
+
Voltage-gated
Na
+
channel
Steady resting membrane potential is near
E
K
, P
K
> P
Na
, due to leak K
+
channels.
2
Local membrane is brought to threshold
voltage by a depolarizing stimulus.
3
Current through opening voltage-gated Na
+
channels rapidly depolarizes the membrane,
causing more Na
+
channels to open.
4
Inactivation of Na
+
channels and delayed
opening of voltage-gated K
+
channels halts
membrane depolarization.
5
Outward current through open voltage-
gated K
+
channels repolarizes the membrane
back to a negative potential.
6
Persistent current through slowly closing
voltage-gated K
+
channels hyperpolarizes
membrane toward E
K
; Na
+
channels return
from inactivated state to closed state(without
opening).
7
Closure of voltage-gated K
+
channels returns
the membrane potential to its resting value.
Voltage-gated
K
+
channel
Resting membrane
potential
Threshold potential
Figure 6–19
The changes in (a) membrane potential (mV) and
(b) relative membrane permeability (P) to sodium
and potassium ions during an action potential. Steps
1–7 are described in more detail in the text.
Figure 6–19
physiological
inquiry
If extracellular [Na
+
] is elevated (and you ignore
any effects of a change in osmolarity), how
would the resting potential and action potential
of a neuron change?
Answer can be found at end of chapter.
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