SYNAPTIC
MORPHOLOGY
Synapses are specialized sites
where neurons communicate with each other and with effector or target cells. A,
A typical neuron that receives numerous synaptic contacts on its cell body
and associated dendrites.
The contacts are derived from both myelinated and
unmyelinated axons. Incoming myelinated axons lose their myelin sheaths,
exhibit extensive branching, and terminate as synaptic boutons (terminals) on
the target (in this example, motor) neuron. B, An enlargement of an
axosomatic terminal. Chemical neurotransmitters are packaged in synaptic
vesicles. When an action potential invades the terminal region, depolarization
triggers Ca2+ influx into the terminal, causing numerous synaptic
vesicles to fuse with the presynaptic membrane, releasing their packets of
neurotransmitter into the synaptic cleft. The neurotransmitter can bind to
receptors on the postsynaptic membrane, resulting in graded excitatory or
inhibitory postsynaptic potentials or in neuromodulatory effects on
intracellular signaling systems in the target cell. There is sometimes a
mismatch between the site of release of a neurotransmitter and the location of
target neurons possessing receptors for the neurotransmitter (can be
immediately adjacent or at a distance). Many nerve terminals can release
multiple neurotransmitters; the process
is regulated by gene activation and by the frequency and duration of axonal
activity. Some nerve terminals possess presynaptic receptors for their released
neurotransmitters. Activation of these presynaptic receptors regulates
neurotransmitter release. Some nerve terminals also possess high-affinity
uptake carriers for transport of the neurotransmitters (e.g. dopamine,
norepinephrine, serotonin) back into the nerve terminal for repackaging and reuse.
CLINICAL POINT
Synaptic endings, particularly
axodendritic and axosomatic endings, terminate abundantly on some neuronal cell
types such as LMNs. The distribution of synapses, based on a hierarchy of
descending pathways and interneurons, orchestrates the excitability of the
target neuron. If one of the major sources of input is disrupted (such as the
corticospinal tract in an internal capsule lesion, which may occur in an
ischemic stroke) or if damage has occurred to the collective descending UMN
pathways (as in a spinal cord injury), the remaining potential sources of input
can sprout and occupy regional sites left bare because of the degeneration of
the normal complement of synapses. As a result, primary sensory inputs from Ia
afferents and other sensory influences, via interneurons, can take on a
predominant influence over the excitability of the target motor neurons,
leading to a hyperexcitable state. This may account in part for the hypertonic
state and hyperreflexic responses to stimulation of primary muscle spindle
afferents (muscle stretch reflex) and of flexor reflex afferents (nociceptive
stimulation). Recent studies indicate that synaptic growth, plasticity, and
remodeling can continue into adulthood and even into old age.
