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In myelinated nerves, the axon between two
nodes of Ranvier (internodal segment) is sur-
rounded by a myelin sheath ( A ). This is a
precondition for saltatory conduction of the
action potentials, i.e., the “jumping” propaga-
tion of excitation from one nodal constriction
(R 1 ) to the next (R 2 ). The internodal segment it-
self cannot generate an action potential, i.e.,
depolarization of the second node (R 2 ) is com-
pletely dependent on the current from the first
node (R 1 ). However, the current is usually so
strong that it can even jump across the nodes.
Nevertheless, on the way along the inter-
nodal segment the amplitude of the current
will diminish. First of all, the membrane in
the internodal segment must change its polar-
ity, i.e., the membrane capacitance must be
discharged, for which a current is needed
( A , green arrow). Secondly, current can also
escape through individual ionic channels in
the axonal membrane (orange arrow). How-
ever, myelination of the internodal segment
causes the membrane resistance (R m ) to be
elevated and the capacity (C m ) of the mem-
brane condensor to be reduced ( A , left).
The resistance of the axonal membrane of
the internodal segment is very high because
of the low density of ionic channels there. Fur-
thermore, the perimembranous space is insu-
lated by a layer of fat from the free extracellu-
lar space. The low capacitance of the conden-
sor is due to the large distance between the in-
terior of the axon and the free extracellular
space as well as the low polarity of the fatty
material in the space between them.
Demyelination ( A , right) can be caused by
degenerative, toxic, or inflammatory damage
to the nerves, or by a deficiency of vitamins B 6
or B 12 . If this happens, R m will be reduced and
C m raised in the internodal segment. As a re-
sult, more current will be required to change
the polarity of the internodal segment (green
arrow) and, through opening up the ionic
channels, large losses of current may occur (or-
ange arrow).
If, after the losses in the internodal seg-
ment, the current generated at R 1 is not ade-
quate to depolarize R 2 to the threshold level,
excitation is interrupted, even though the
axon is completely intact. High frequency of
action potentials and low temperature favor
interruption of conduction because of decreas-
ing sensitivity of the node R 2 ( A 1 ). Minor le-
sions of the internodal segment can lead to
slowing of conduction, because it can no lon-
ger jump across nodes and the next node has
to be depolarized to its threshold before the
excitation is passed to the afternext nodes
( A 2 ). The resulting slowing may not be the
same in different fibers, so that temporal dis-
persion of the signal may occur. Lastly, the
damaged site may itself trigger action poten-
tials, especially when the axon has concomi-
tantly suffered spontaneous damage or is un-
der mechanical pressure ( A 3 ); excitation
can jump across two neighboring damaged
nerve fibers (ephaptic transmission; A 4 ), or
conduction may run retrogradely ( A 5 ).
Genetic defects of the myelin-sheath pro-
tein (e.g., protein O [P 0 , of peripheral myelin
protein 22 (PMP 22)]) or of gap junctions in
the Schwann cells (connexin 22) lead to cer-
tain hereditary peripheral neuropathies ( Char-
cot-Marie-Tooth syndrome , Dejerine-Sottas
syndrome, Pelizaeus-Merzbacher disease).
The most important demyelinating disease
is multiple sclerosis ( B ). It is more common
in women than men, familial aggregation
sometimes occurs, and it has a higher inci-
dence among carriers of HLA3 and HLA7. It is
an autoimmune disease that may be triggered
by a viral infection and is characterized by de-
myelinating inflammatory foci ( B 1 ). The
typical feature of multiple sclerosis is the tem-
porally unrelated occurrence of completely
different neuronal deficits, caused by lesions
in different parts of the brain. Some of the le-
sions may partly regress when the local in-
flammatory process has subsided and the
nerves (in the case of intact axons) have been
remyelinated. The example in B 2 illustrates
that at first there is a fully reversible loss of vi-
sion due to a damaged optic nerve ( p. 326),
followed by a partly reversible sensory loss
when the sensory tracts of the spinal cord are
affected ( p. 318). Finally, ataxia sets in when
the cerebellum becomes involved ( p. 316).
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