168 Chapter 7
cell wraps only about a millimeter of axon, leaving gaps of
exposed axon between the adjacent Schwann cells. These gaps
in the myelin sheath are known as the nodes of Ranvier. The
successive wrappings of Schwann cell membrane provide
insulation around the axon, leaving only the nodes of Ranvier
exposed to produce nerve impulses.
The Schwann cells remain alive as their cytoplasm is forced
to the outside of the myelin sheath. As a result, myelinated axons
of the PNS are surrounded by a living sheath of Schwann cells,
or neurilemma ( figs. 7.6 and 7.7 ). Unmyelinated axons are also
surrounded by a neurilemma, but they differ from myelinated
axons in that they lack the multiple wrappings of Schwann cell
plasma membrane that compose the myelin sheath.
Myelin Sheath in CNS
As mentioned earlier, the myelin sheaths of the CNS are
formed by oligodendrocytes. This process occurs mostly post-
natally (after birth) and continues into late adolescence. It may
continue later into adulthood in some brain regions, and there
is evidence that learning certain activities (such as playing
piano), particularly in childhood, may increase myelination.
CLINICAL APPLICATION
Demyelinating diseases are those in which the myelin sheaths
are specifically attacked. Because Schwann cells form the
myelin in the PNS, whereas oligodendrocytes form the myelin
of the CNS, the immune system attacks one or the other type of
myelin. In Guillain-Barre syndrome, the T cells of the immune
system (chapter 15) attack myelin sheaths of the PNS. This pro-
duces rapid onset of symptoms that include muscle weakness
(which can dangerously affect the muscles of breathing) due
to dysfunction of somatic motor axons, and cardiac and blood
pressure problems due to dysfunction of autonomic axons.
Multiple sclerosis ( MS ) is produced by autoimmune
attack (chapter 15, section 15.6) mediated by T cells on the
myelin sheaths in the CNS. This leads to areas of hardening, or
scleroses, followed by axonal degeneration. MS is usually diag-
nosed in people between the ages of 20 and 40, and is twice
as common among woman than men. It is a chronic remitting
and relapsing disease with highly variable symptoms, including
sensory impairments, motor dysfunction and spasticity, blad-
der and intestinal problems, fatigue, and others. Treatment for
MS includes drugs that reduce autoimmune activity and inflam-
mation, and drugs that interfere with the entry of autoreactive
T cells into the CNS. These drugs help in treating the symptoms
of MS, but do not restore myelin sheaths or cure the disease.
Myelin sheath
Schwann cellSchwann cell
cytoplasmcytoplasm
Schwann cell
cytoplasm
MyelinatedMyelinated
axonaxon
Myelinated
axon
UnmyelinatedUnmyelinated
axonaxon
Unmyelinated
axon Schwann cellSchwann cell
cytoplasmcytoplasm
Schwann cell
cytoplasm
Figure 7.7 An electron micrograph of unmyelinated
and myelinated axons. Notice that myelinated axons have
Schwann cell cytoplasm to the outside of their myelin sheath,
and that Schwann cell cytoplasm also surrounds unmyelinated
axons.
Figure 7.8 The formation of myelin sheaths in the
CNS by an oligodendrocyte. One oligodendrocyte forms
myelin sheaths around several axons.
Oligodendrocyte
Node of Ranvier
Axon
Myelin
sheath
Unlike a Schwann cell, which forms a myelin sheath around
only one axon, each oligodendrocyte has extensions, like the
tentacles of an octopus, that form myelin sheaths around several
axons ( fig. 7.8 ). The myelin sheaths around axons of the CNS