Figure 9.8
When a nerve impulse
reaches a neuromuscular junction,
acetylcholine (ACh) is released. Upon
binding to sarcolemma receptors,
ACh causes a change in sarcolemma
permeability leading to a change in
membrane potential.
Action
potential (AP)
Myelinated axon
of motor neuron
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Ca
2+
Ca
2+
Axon terminal
of motor neuron
Synaptic vesicle
containing ACh
Synaptic cleft
Junctional
folds of
sarcolemma
Fusing
synaptic
vesicles
ACh
Sarcoplasm of
muscle fiber
Postsynaptic membrane
ion channel opens;
ions pass.
Na
+
K
+
ACh
Na
+
K
+
Degraded ACh
Acetylcholinesterase
Ion channel closes;
ions cannot pass.
1
Action potential arrives at
axon terminal of motor neuron.
2
Voltage-gated Ca
2+
channels open. Ca
2+
enters the
axon terminal moving down its
electochemical gradient.
3
Ca
2+
entry causes ACh (a
neurotransmitter) to be released
by exocytosis.
4
ACh diffuses across the
synaptic cleft and binds to its
receptors on the sarcolemma.
5
ACh binding opens ion
channels in the receptors that
allow simultaneous passage of
Na
+
into the muscle fiber and K
+
out of the muscle fiber. More Na
+
ions enter than K
+
ions exit,
which produces a local change in
the membrane potential called
the end plate potential.
6
ACh effects are terminated by
its breakdown in the synaptic
cleft by acetylcholinesterase and
diffusion away from the junction.
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Events at the Neuromuscular Junction
 
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