In the summer months of the early 1950s, millions of children con-
tracted poliomyelitis, a viral infection that attacks motor neurons.
Fever, headache, and nausea rapidly progressed to a sti±
ened back
and neck, drowsiness, and then paralysis, usually of the lower limbs
or muscles that control breathing or swallowing.
Vaccines introduced in the middle 1950s vanquished polio in
many nations, but the disease resurged in Nigeria in 2003, where
rumors that the vaccine causes female infertility led to a boycott of the
World Health Organization’s Global Polio Eradication Initiative. Polio
has spread to neighboring nations and to as far away as Indonesia.
In the United States, a third of the 1.6 million polio survivors suf-
fer the fatigue, muscle weakness and atrophy, and di²
culty breath-
ing of postpolio syndrome. Researchers think that in this condition,
surviving motor neurons that grew extra axon branches to compen-
sate for neurons lost during polio degenerate from years of overuse.
Stimulus for Contraction
Acetylcholine (ACh)
is the neurotransmitter that motor neu-
rons use to control skeletal muscle contraction. ACh is syn-
thesized in the cytoplasm of the motor neuron and is stored in
synaptic vesicles near the distal end of its axon. When a nerve
impulse (a series of action potentials, described in chapter 10,
pp. 369–370) reaches the end of the axon, some of these vesi-
cles release acetylcholine into the synaptic cleft (see F g. 9.8).
Acetylcholine diffuses rapidly across the synaptic cleft and
binds to speciF c protein molecules (receptors) in the muscle
fiber membrane, increasing the membrane permeability to
sodium ions. The entry of these charged particles into the mus-
cle cell stimulates a
muscle impulse
(a series of action poten-
tials), an electrical signal very much like a nerve impulse. A
muscle impulse changes the muscle cell membrane in a way
that transmits the impulse in all directions along and around the
muscle cell, into the transverse tubules, into the sarcoplasm,
and ultimately to the sarcoplasmic reticulum and the cisternae.
Clinical Application 9.1 discusses myasthenia gravis, in which
the immune system attacks certain neuromuscular junctions.
The site where an axon and a muscle F
ber meet is called
neuromuscular junction
(myoneural junction). There, the
muscle F ber membrane is specialized to form a
motor end
where nuclei and mitochondria are abundant and the
sarcolemma is extensively folded
g. 9.8)
A muscle fiber usually has a single motor end plate.
Motor neuron axons, however, are densely branched, which
enables one such axon to connect to many muscle F
Together, a motor neuron and the muscle F bers it controls
constitute a
motor unit
tor u
g. 9.9)
A small gap called the
synaptic cleft
separates the mem-
brane of the neuron and the membrane of the muscle F ber.
The cytoplasm at the distal ends of the nerve F ber is rich
in mitochondria and contains many tiny vesicles (synaptic
vesicles) that store neurotransmitters.
Neuromuscular junction. (
) A neuromuscular junction
includes the end of a motor neuron and the motor end plate of a
muscle ³
ber. (
) Micrograph of a neuromuscular junction (500×).
neuron axon
end plate
Axon branches
Muscle fiber
Myofibril of
muscle fiber
Motor neuron axon
Muscle fiber
Neuromuscular junction
Motor neuron
of motor unit 1
Motor neuron
of motor unit 2
Skeletal muscle
Branches of
motor neuron
Two motor units. The muscle ³
bers of a motor unit are
innervated by a single motor neuron and may be distributed throughout
the muscle.
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