164
Chapter 6
In the previous examples, we referred to the threshold
of the postsynaptic neuron as though it were the same for all
parts of the cell. However, different parts of the neuron have
different thresholds. In general, the initial segment has a lower
threshold (i.e., much closer to the resting potential) than the
membrane of the cell body and dendrites. This is due to a
higher density of voltage-gated sodium channels in this area
of the membrane. Therefore, the initial segment is extremely
responsive to small changes in the membrane potential that
occur in response to synaptic potentials on the cell body and
dendrites. The initial segment reaches threshold whenever
enough EPSPs summate. The resulting action potential is
then propagated from this point down the axon.
The fact that the initial segment usually has the lowest
threshold explains why the locations of individual synapses on
the postsynaptic cell are important. A synapse located near the
initial segment will produce a greater voltage change in the
initial segment than will a synapse on the outermost branch
of a dendrite because it will expose the initial segment to a
larger local current. In some neurons, however, signals from
dendrites distant from the initial segment may be boosted by
the presence of some voltage-gated sodium channels in parts
of those dendrites.
Postsynaptic potentials last much longer than action
potentials. In the event that cumulative EPSPs cause the ini-
tial segment to still be depolarized to threshold after an action
potential has been fi red and the refractory period is over, a
second action potential will occur
. In fact, as long as the
membrane is depolarized to threshold, action potentials will
continue to arise. Neuronal responses almost always occur in
bursts of action potentials rather than as single, isolated events.
Synaptic Strength
Individual synaptic events—whether excitatory or inhibitory—
have been presented as though their effects are constant and
reproducible. Actually, enormous variability occurs in the post-
synaptic potentials that follow a presynaptic input. The effec-
tiveness or strength of a given synapse is infl uenced by both
presynaptic and postsynaptic mechanisms.
A presynaptic terminal does not release a constant
amount of neurotransmitter every time it is activated. One rea-
son for this variation involves calcium concentration. Calcium
that has entered the terminal during previous action potentials
is pumped out of the cell or (temporarily) into intracellular
organelles. If calcium removal does not keep up with entry, as
can occur during high-frequency stimulation, calcium concen-
tration in the terminal, and consequently the amount of neu-
rotransmitter released upon subsequent stimulation, will be
greater than usual. The greater the amount of neurotransmit-
ter released, the greater the number of ion channels opened in
the postsynaptic membrane, and the larger the amplitude of
the EPSP or IPSP in the postsynaptic cell.
The neurotransmitter output of some presynaptic termi-
nals is also altered by activation of membrane receptors on the
terminals themselves. Activation of these presynaptic receptors
infl uences calcium infl ux into the terminal and thus the num-
ber of neurotransmitter vesicles that release neurotransmitter
into the synaptic cleft. These presynaptic receptors may be asso-
ciated with a second synaptic ending known as an
axo-axonic
synapse,
in which an axon terminal of one neuron ends on an
axon terminal of another. For example, in
Figure 6–33
the neu-
rotransmitter released by A binds with receptors on B, resulting
in a change in the amount of neurotransmitter released from B
in response to action potentials. Thus, neuron A has no direct
effect on neuron C, but it has an important infl uence on the
ability of B to infl uence C. Neuron A is thus exerting a presyn-
aptic effect on the synapse between B and C. Depending upon
the type of presynaptic receptors activated by the neurotrans-
mitter from neuron A, the presynaptic effect may decrease the
amoun
t
o
f
neurotransm
i
tter
re
leased
from
B
(presynaptic
inhibition)
or increase it
(presynaptic facilitation).
Axo-axonic synapses such as A in Figure 6–33 can alter
the calcium concentration in axon terminal B or even affect
neurotransmitter synthesis there. If the calcium concentration
increases, the number of vesicles releasing neurotransmitter
from B increases. Decreased calcium reduces the number of
vesicles releasing transmitter. Axo-axonic synapses are impor-
tant because they selectively control one specifi c input to the
postsynaptic neuron C. This type of synapse is particularly
common in the modulation of sensory input.
Figure 6–32
Comparison of excitatory and inhibitory synapses, showing
current direction through the postsynaptic cell following synaptic
activation. (a) Current through the postsynaptic cell is away from
the excitatory synapse, and may depolarize the initial segment.
(b) Current through the postsynaptic cell is toward the inhibitory
synapse and may hyperpolarize the initial segment. The arrow on
the chart indicates moment of stimulus.
Membrane potential
Membrane potential
Time
Time
Initial segment
Initial segment
(a) Excitatory synapse
(b) Inhibitory synapse
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
previous page 192 Vander's Human Physiology The Mechanisms of Body Function read online next page 194 Vander's Human Physiology The Mechanisms of Body Function read online Home Toggle text on/off