Individual Neurons - Computational Explorations in Cognitive Neuroscience - page 34

on the level of the membrane potential) that plays a
central role in triggering the action potential, as de-
scribed previously. In general, Na + plays the central
role in the excitation or activation of the neuron, be-
cause diffusion forces tend to push it into the neuron,
resulting in the elevation of the membrane potential.
Excitation is also referred to as depolarization ,be-
cause it makes the membrane potential less polarized
(i.e., closer to having a 0mV potential).
Cl ￿ Because of the negative resting potential cre-
ated by the sodium-potassium pump, the negatively
charged chloride ions are repelled out of the neuron,
resulting in a concentration imbalance with more ions
outside than inside. Thus, as with Na + , the diffusion
force pushes Cl ￿ into the neuron. However, this dif-
fusion force is exactly counteracted by the negative
resting potential, which creates the imbalance in the
first place, so that the equilibrium potential for Cl ￿
is just the resting potential of the neuron, typically

the negative resting potential, so that its equilibrium
potential is typically around ￿90mV .
There are many different types of K + channels, but
the most relevant for our purposes is the leak channel,
which is constantly open and lets out small amounts
of potassium. However, this channel also lets in small
amounts of Na + , so that the equilibrium potential for
the conductance of this channel is not quite the same
as that for the K + ion — it is instead the same as
the resting potential, or roughly ￿70mV .Thereis
also a voltage-gated K + channel that counteracts the
effects of the excitation produced during the action
potential by letting out larger amounts of K + when
the neuron becomes very excited. A third type of
K + channel opens as a function of the amount of cal-
cium ion present in a neuron, which is indicative of
extended periods of activity. Thus, this channel pro-
duces an accommodation or fatiguelike effect by in-
hibiting overactive neurons, as discussed further in
the last section of this chapter. In general, K + plays
alargely regulatory role in the neuron.
Ca ++ The calcium ion is present in only minute con-
centrations inside the neuron due to another type of
active pump that pumps Ca ++ out, and other intra-
cellular mechanisms that absorb or buffer calcium.
Thus, the diffusion force on Ca ++ is inward, re-
quiring a positive internal potential to push it back
out.

.
The main Cl ￿ channel is the inhibitory synaptic in-
put channel that is opened by the neurotransmitter
GABA as described previously. Note that because
the equilibrium potential for Cl ￿ is the same as the
resting potential, the inhibition delivered by these
neurons does not have much of an effect (i.e., not
much current is generated) until the neuron starts to
get excited and its membrane potential rises. This
phenomenon is often described as shunting inhibi-
tion.
K + The concentration of potassium is a function of
both the direct and indirect effects of the sodium-
potassium pump. The direct effect is that some
amount of K + is actively pumped into the cell. In
addition, the fact that the pump results in a negative
resting potential will cause this positively charged ion
to be drawn into the neuron as well. Thus, there
is a much greater concentration of potassium inside
than outside the cell. As a result, its diffusion force
pushes it out of the neuron (unlike the previous two
ions). This diffusion force is mostly countered by the
negative resting potential, but because it is also ac-
tively pumped into the neuron, its internal concentra-
tion is even higher than would be expected from just

This potential is somewhere on the order of

, due to the relatively large concentration
differences involved. Note also that by having two
extra positive charges instead of one, a given electri-
cal potential acts twice as strongly on this ion as on
ions with only one net charge difference.
Perhaps the most important channel that conducts
Ca ++ is the NMDA channel, triggered by glutamate
released by excitatory neurons as mentioned previ-
ously. This channel is critical for the learning mecha-
nisms described in chapters 4-6. Also, the accom-
modation effect (and its opposite, the sensitization
effect) depends on the presence of Ca ++ ions in the
neuron as a measure of neural activity. These ions
enter the neuron through voltage-gated channels, so
that their presence indicates recent neural activity,
and they exist in such small amounts in the neuron