Neuronal Signaling and the Structure of the Nervous System
165
Some receptors on the presynaptic terminal are not asso-
ciated with axo-axonic synapses. Instead, they are activated by
neurotransmitters or other chemical messengers released by
nearby neurons or glia or even by the axon terminal itself. In
the last case, the receptors are called
autoreceptors
(Figure
6–33) and provide an important feedback mechanism the
neuron can use to regulate its own neurotransmitter output.
In most cases, the released neurotransmitter acts on autore-
ceptors to decrease its own release, thereby providing negative
feedback control.
Postsynaptic
mechanisms for varying synaptic strength
also exist. For example, as described in Chapter 5, many types
and subtypes of receptors exist for each kind of neurotrans-
mitter. The different receptor types operate by different sig-
nal transduction mechanisms and have different—sometimes
even opposite—effects on the postsynaptic mechanisms they
infl uence. Moreover, a given signal transduction mechanism
may be regulated by multiple neurotransmitters, and the vari-
ous second-messenger systems affecting a channel may inter-
act with each other.
Recall, too, from Chapter 5 that the number of recep-
tors is not constant, varying with up- and down-regulation,
for example. Also, the ability of a given receptor to respond
to its neurotransmitter can change. Thus, in some systems, a
receptor responds once and then temporarily fails to respond
despite the continued presence of the receptor’s neurotrans-
mitter, a phenomenon known as
receptor desensitization.
Imagine the complexity when a cotransmitter (or sev-
eral cotransmitters) is released with the neurotransmitter to
act upon postsynaptic receptors and maybe upon presynaptic
receptors as well! Clearly, the possible variations in transmission
are great at even a single synapse, and this provides a mecha-
nism by which synaptic strength can be altered in response to
changing conditions, a characteristic known as
plasticity.
Modifi
cation of Synaptic Transmission by
Drugs and Disease
The great majority of drugs that act on the nervous system do
so by altering synaptic mechanisms and thus synaptic strength.
Drugs act by interfering with or stimulating normal processes
in the neuron involved in neurotransmitter synthesis, storage,
and release, and in receptor activation. The synaptic mecha-
nisms labeled in
Figure 6–34
are important to synaptic func-
tion and are vulnerable to the effects of drugs.
The long-term effects of drugs are sometimes diffi
cult
to predict because the imbalances the initial drug action pro-
duces are soon counteracted by feedback mechanisms that
normally regulate the processes. For example, if a drug inter-
feres with the action of a neurotransmitter by inhibiting the
rate-limiting enzyme in its synthetic pathway, the neurons may
respond by increasing the rate of precursor transport into the
axon terminals to maximize the use of any available enzyme.
A
C
Presynaptic
receptor
Autoreceptor
B
Postsynaptic receptor
Figure 6–33
A presynaptic (axo-axonic) synapse between axon terminal A and
axon terminal B. C is the fi nal postsynaptic cell body.
Direction of action potential
propagation
Synthesizing
enzyme
F
A
D
E
B
C
Postsynaptic neuron
Presynaptic
neuron
Neurotransmitter
precursors
Vesicle
Degrading
enzymes
Synaptic
cleft
Reuptake
G
H
Figure 6–34
Possible actions of drugs on a synapse. A drug might: (A) Increase
leakage of neurotransmitter from vesicle to cytoplasm, exposing it
to enzyme breakdown, (B) increase transmitter release into cleft,
(C) block transmitter release, (D) inhibit transmitter synthesis,
(E) block transmitter reuptake, (F) block cleft enzymes that
metabolize transmitter, (G) bind to receptor on postsynaptic
membrane to block (antagonist) or mimic (agonist) transmitter
action, and (H) inhibit or stimulate second-messenger activity
within postsynaptic cell.
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