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SYNAPTIC MORPHOLOGY


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.
SYNAPTIC MORPHOLOGY

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.