MYELINATION OF CNS AND PNS AXONS
Central myelination of axons is provided by
oligodendroglia. Each oligodendroglial cell can myelinate a single segment of
several separate central axons. In the PNS, sensory, motor, and preganglionic
autonomic axons are myelinated by Schwann cells. A Schwann cell myelinates only
a single segment of one axon. Unmyelinated sensory and autonomic postganglionic
autonomic axons are ensheathed by a Schwann cell, which provides a single
enwrapping arm of cytoplasm around each of several such axons. The space
between adjacent myelin segments of an axon is called a node of Ranvier; this
site of axon membrane contains sodium channels and allows the reinitiation of
action potentials in the course of propagation down the axon, a process called
saltatory conduction.
CLINICAL POINT
The integrity of the myelin sheath is essential for proper
neuronal function in both the CNS and the PNS. Disruption of the myelin sheath around
axons in either system results in the inability of the formerly myelinated
axons to carry out their functional activities. In the CNS, the myelin sheath
of central axons can be attacked in an autoimmune disease such as multiple
sclerosis, resulting in a variety of symptoms, such as blindness, diplopia
caused by discoordinated eye movements, loss of sensation, loss of
coordination, paresis, and others. This condition may occur episodically, with
intermittent remyelination occurring as the result of oligodendroglia
proliferation and remyelination. In the PNS, a wide variety of insults,
including exposure to toxins and the presence of diabetes or autoimmune
Guillain-Barré syndrome, result in peripheral axonal demyelination, which is
manifested mainly as sensory loss and paralysis or weakness. Remyelination also
can occur around peripheral axons, initiated by the Schwann cells. Clinically,
the status of axonal conduction is assessed by examining sensory evoked potentials
in the CNS and by conduction velocity studies in the PNS.
