or disorders (Table 8–1 summarizes the functions of
the neuroglia).
SYNAPSES
Neurons that transmit impulses to other neurons do
not actually touch one another. The small gap or space
between the axon of one neuron and the dendrites or
cell body of the next neuron is called the synapse.
Within the synaptic knob (terminal end) of the presy-
naptic axon is a chemical neurotransmitterthat is
released into the synapse by the arrival of an electrical
nerve impulse (Fig. 8–2). The neurotransmitter dif-
fuses across the synapse, combines with specific recep-
tor sites on the cell membrane of the postsynaptic
neuron, and there generates an electrical impulse that
is, in turn, carried by this neuron’s axon to the next
synapse, and so forth. A chemical inactivatorat the
cell body or dendrite of the postsynaptic neuron
quickly inactivates the neurotransmitter. This pre-
vents unwanted, continuous impulses, unless a new
impulse from the first neuron releases more neuro-
transmitter.
Many synapses are termed excitatory, because the
neurotransmitter causes the postsynaptic neuron to
depolarize (become more negative outside as Naions
enter the cell) and transmit an electrical impulse to
another neuron, muscle cell, or gland. Some synapses,
however, are inhibitory, meaning that the neurotrans-
mitter causes the postsynaptic neuron to hyperpolar-
ize (become even more positive outside as K ions
leave the cell or Clions enter the cell) and therefore
not transmit an electrical impulse. Such inhibitory
synapses are important, for example, for slowing the
heart rate, and for balancing the excitatory impulses
transmitted to skeletal muscles. With respect to the
skeletal muscles, this inhibition prevents excessive
contraction and is important for coordination.168 The Nervous System
BOX8–1 MULTIPLE SCLEROSIS
protect the axon. Because loss of myelin may
occur in many parts of the central nervous system,
the symptoms vary, but they usually include muscle
weakness or paralysis, numbness or partial loss
of sensation, double vision, and loss of spinal
cord reflexes, including those for urination and
defecation.
The first symptoms usually appear between the
ages of 20 and 40 years, and the disease may
progress either slowly or rapidly. Some MS patients
haveremissions, periods of time when their symp-
toms diminish, but remissions and progression of
the disease are not predictable. There is still no cure
for MS, but therapies include suppression of the
immune response, and interferon, which seems to
prolong remissions in some patients. The possibility
of stimulating remyelination of neurons is also
being investigated.Multiple sclerosis (MS) is a demyelinating dis-
ease; that is, it involves deterioration of the myelin
sheath of neurons in the central nervous system.
Without the myelin sheath, the impulses of these
neurons are short-circuited and do not reach their
proper destinations, and the neuron axons are
damaged and gradually die.
Multiple sclerosis is an autoimmunedisorder
that may be triggered by a virus or bacterial infec-
tion. Research has also uncovered a genetic com-
ponent to some clusters of MS cases in families.
Exactly how such genes would increase a person’s
susceptibility to an autoimmune disease is not
yet known. In MS, the autoantibodies destroy
the oligodendrocytes, the myelin-producing neu-
roglia of the central nervous system, which results
in the formation of scleroses, or plaques of scar
tissue, that do not provide electrical insulation orTable 8–1 NEUROGLIAName Function
OligodendrocytesMicrogliaAstrocytesEpendyma- Produce the myelin sheath to
electrically insulate neurons of
the CNS. - Capable of movement and
phagocytosis of pathogens
and damaged tissue. - Support neurons, help main-
tain Klevel, contribute to the
blood–brain barrier. - Line the ventricles of the
brain; many of the cells have
cilia; involved in circulation of
cerebrospinal fluid.