286
UNIT 2
Covering, Support, and Movement of the Body
9
As a rule, each muscle fiber has only one neuromuscular
junction, located approximately midway along its length. Te
axon terminal and the muscle fiber are exceedingly close (50–
80 nm apart), but they remain separated by a space, the
synap-
tic clef
(Figure 9.8), which is filled with a gel-like extracellular
substance rich in glycoproteins and collagen fibers.
Within the moundlike axon terminal are
synaptic vesicles
,
small membranous sacs containing the neurotransmitter
ace-
tylcholine
(as
0
ĕ-til-ko
9
lēn), or
ACh
. Te trough-like part of
the muscle fiber’s sarcolemma that helps form the neuromus-
cular junction is highly folded. Tese
junctional Folds
provide
a large surface area for the millions of
ACh receptors
located
there. Hence, the neuromuscular junction includes the axon
terminals, the synaptic cle±, and the junctional folds of the
sarcolemma.
How does a motor neuron stimulate a skeletal muscle fiber?
Te simplest explanation is:
When a nerve impulse reaches the end of an axon, the axon
terminal releases ACh into the synaptic cle±.
ACh diffuses across the cle± and attaches to ACh receptors
on the sarcolemma of the muscle fiber.
ACh binding triggers electrical events that ultimately gener-
ate an action potential.
Focus on Events at the Neuromuscular Junction
(Figure 9.8)
covers this process step by step. Study this figure before
continuing.
A±er ACh binds to the ACh receptors, its effects are quickly
terminated by
acetylcholinesterase
(as
0
ĕ-til-ko
0
lin-es
9
ter-ās),
an enzyme located in the synaptic cle±. Acetylcholinesterase
breaks down ACh to its building blocks, acetic acid and choline.
Tis removal of ACh prevents continued (and most likely un-
desirable) muscle fiber contraction in the absence of additional
nervous system stimulation.
Homeostatic Imbalance
9.1
Many toxins, drugs, and diseases interfere with events at the
neuromuscular junction. For example,
myasthenia gravis
(
asthen
5
weakness;
gravi
5
heavy), a disease characterized
by drooping upper eyelids, difficulty swallowing and talking,
and generalized muscle weakness, involves a shortage of ACh
receptors. Serum analysis reveals antibodies to ACh receptors,
suggesting that myasthenia gravis is an autoimmune disease.
Although normal numbers of receptors are initially present,
they appear to be destroyed as the disease progresses.
Generation of an Action Potential
Across the Sarcolemma
Like the plasma membranes of all cells, a resting sarcolemma is
polarized
. Tat is, a voltmeter would show there is a potential
difference (voltage) across the membrane and the inside is nega-
tive relative to the outer membrane face. (Chapter 3 describes
the resting membrane potential.)
An action potential (AP) is the result of a predictable se-
quence of electrical changes. Once initiated, they occur along
3. Te action potential is automatically propagated along the
sarcolomma.
4. Ten, intracellular calcium ion levels must rise briefly,
providing the final trigger for contraction.
Steps 1 and 2, activation, occur at the neuromuscular junction
and set the stage for the events that follow. Steps 3 and 4, which
link the electrical signal to contraction, are called excitation-
contraction coupling.
Figure 9.7
summarizes this series of
events into two major phases, which we consider in detail below.
The Nerve Stimulus and Events at the
Neuromuscular Junction
Te nerve cells that activate skeletal muscle fibers are called
so-
matic motor neurons
, or
motor neurons of the somatic
(
volun-
tary
)
nervous system
. Tese motor neurons “reside” in the brain
or spinal cord, but their long threadlike extensions called axons
travel, bundled within nerves, to the muscle cells they serve.
Te axon of each motor neuron divides profusely as it enters
the muscle. Each axon ending gives off several short, curling
branches that collectively form an elliptical
neuromuscular
junction
, or
end plate
, with a single muscle fiber.
Phase 1
Motor neuron
stimulates
muscle fiber
(see Figure 9.8).
Action potential (AP) arrives at axon
terminal at neuromuscular junction
ACh released; binds to receptors
on sarcolemma
Ion permeability of sarcolemma changes
Local change in membrane voltage
(depolarization) occurs
Local depolarization (end plate
potential) ignites AP in sarcolemma
AP travels across the entire sarcolemma
AP travels along T tubules
SR releases Ca
2+
; Ca
2+
binds to
troponin; myosin-binding sites
(active sites) on actin exposed
Myosin heads bind to actin;
contraction begins
Phase 2:
Excitation-contraction
coupling occurs (see
Figures 9.9 and 9.11).
Figure 9.7
The phases leading to muscle fiber contraction.
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