106
UNIT 2
Basic Tissues
Figure 6-6A.
Motor endplates on skeletal muscle.
Silver
stain,
3
83; inset
3
184
A motor nerve (
black
) is shown terminating on skeletal
muscle
f bers (
violet
). The nerve contains several dozen individual
axons
, which leave the nerve and Form multiple
motor end-
plates
. These endplates are the sites oF the
neuromuscular junc-
tions
, where the axon makes synaptic contact with individual
muscle f bers. A single axon contacts numerous muscle f bers.
The motor neuron, its associated axon, and all oF the muscle
f bers that it contacts are def
ned as a
motor unit
. Each time an
action potential travels along the axon and causes the release
oF
Ach
at the neuromuscular junction, a contraction is pro-
duced in the muscle f bers innervated by that axon. In small
muscles involved in f ne movements, a single axon may contact
10 to 100 muscle f bers; in large muscles, which produce great
Force, the motor units may include 500 to 1,000 muscle f bers.
Motor nerve
Motor nerve
Motor
Motor
endplate
endplate
Single axons
Single axons
Motor nerve
Muscle fibers
Single axons
Motor
endplate
A
Voltage-gated
channel
Transmitter-gated
channel
Synaptic vesicle
Axon terminal
Schwann cell
Subjunctional fold
Synaptic cleft
Motor
endplate
B
Figure 6-6B.
Neuromuscular junction.
A single motor endplate (
red circle in inset
) is shown in cross
section. The nervous system controls muscle contraction using a
combination oF electrical and chemical signals. When an action
potential travels to the end oF an axon, the associated electrical
charge causes the
synaptic vesicles
clustered in the axon terminal to
release a
neurotransmitter
,
ACh
, into the
synaptic cleft
. The ACh
acts upon
receptors
in
transmitter-gated ion channels
(
blue
) in the
postsynaptic membrane. When the channels open, a voltage change
occurs across the membrane, which, in turn, activates
voltage-gated
channels
(
red
) in the sarcolemma. This voltage change sweeps rap-
idly along the sarcolemma and invades the T-tubule system, in
which it causes the release oF calcium ions and consequent muscle
contraction. The
subjunctional folds
in the postsynaptic membrane
serve as a reservoir For the enzyme acetylcholinesterase, which rap-
idly inactivates the ACh aFter each transmitter release.
CLINICAL CORRELATION
Figure 6-6C.
Myasthenia Gravis
Myasthenia gravis
is an
autoimmune disease
that aFFects
the neuromuscular junction, causing fl
uctuating weakness
and Fatigue oF skeletal muscles, including ocular,
bulbar,
limb, and respiratory muscles.
Acetylcholine receptor
antibodies
, which block and attack ACh receptors in the
postsynaptic membrane oF the neuromuscular junction,
are the most common causes, especially For patients who
develop the disease in adolescence and adulthood. The
mechanism may involve
thymic hyperplasia
, the binding
oF T lymphocytes to ACh receptors to stimulate B cells to
produce autoantibodies, or genetic deFects. This illustra-
tion shows Fewer ACh receptors than normal, reduction
in subjunctional Fold depth, and increased synaptic cleFt
width. Treatments include using anticholinesterase agents,
immunosuppressive agents, and
thymectomy
(surgical
excision oF the thymus).
J.Lynch
T. Yang
Voltage-gated
channel
Fewer ACh receptors
(transmitter-gated
channels)
Synaptic vesicle
Axon terminal
Schwann cell
Shallower
subjunctional folds
Wider
synaptic cleft
C
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