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Number 190
Neuromuscular Junctions
This Factsheet describes recent exam questions on the events that occur when a nerve impulse reaches a muscle.
Fig.1 Neuromuscular junction.
Myelin sheath
Exam Hint: Make sure that you can
label this diagram
Motor neurone
Mitochondria provide ATP for
synthesis of neurotransmitter
Synaptic bulb
Synaptic vesicles
(containing neurotransmitter)
Presynaptic membrane
Synaptic cleft
Cytoplasm of
muscle fibre
Postsynaptic
membrane
(sarcolemma)
Myofibril
One sarcomere
Nerve impulses arriving at the neuromuscular junction result in shortening of sarcomeres. The classic first type of exam question simply
asks you to explain how.
You must learn these key points:
1 The presynaptic membrane is depolarized.
2 Ca2+ channels on the presynaptic membrane open.
3 There is an Influx of Ca2+2 ions from the synaptic cleft into the
synaptic bulb.
4 Vesicles move towards presynaptic membrane.
5 Vesicles fuse with presynaptic membrane.
6 Neurotransmitter e.g. acetylcholine is released from the vesicles.
7 The neurotransmitter diffuses across the gap or synaptic cleft.
8 The neurotransmitter binds to protein receptors on the
sarcolemma (post-synaptic membrane)which has a large surface
area for this purpose.
9 The binding of the neurotransmitter to the receptors on the
sarcolemma causes sodium channels to open causing an influx
of sodium ions.
10 An action potential is generated and there is depolarization
along the surface of the muscle/depolarisation spreads down
transverse tubules.
11 Calcium channels in the sarcoplasmic reticulum open.
12 Calcium ions diffuse out and bind to troponin.
13 Troponin moves tropomyosin.
• Many candidates believe that it is the calcium that moves
tropomyosin – it isn’t
14 This exposes myosin binding sites on actin molecules / thin
filaments
15 The calcium ions activate myosin which releases ATPase to
split ATP from mitochondria into ADP and Pi
16 This energy is used to move the heads of the myosin filaments
towards the now exposed binding sites on actin
17 The myosin head binds to the binding site on actin and cross
bridges are formed
18 The myosin heads tilt pulling the actin filaments past them
19 As they slide, the heads detach from one site and bind to the
next in a ratchet mechanism
20 As actin filaments from either end of the sarcomere move
towards each other, the muscle fibre contracts/ there is greater
overlap between thick and thin filaments
21 The sarcomere shortens / the distance between Z discs
decreases
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Bio Factsheet
190. Neuromuscular Junctions
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Applying this knowledge
Extract from Chief Examiner's Reports
Once you have learned and understood these basic facts, you
should be ready to tackle questions which ask you to apply this
knowledge.
What candidates get wrong on this first part
• Many candidates stated that vesicles move across the cleft
• Ion movement was often poorly described, with the direction
of movement often omitted. Many candidates incorrectly
referred to movement of chlorine or sodium ions at the
presynaptic knob
• Many candidates failed to mention binding to receptors on
the postsynaptic membrane
• Some made reference to depolarisation of the neurone rather
than the membrane
The cobra is a very poisonous snake.
The molecular structure of cobra toxin
is similar to the molecular structure of
acetylcholine. The toxin permanently
prevents muscle contraction.
How?
Because the toxin is structurally similar to acetylcholine, it competes
for and blocks the acetylcholine receptors. This means that
acetylcholine cannot depolarise the membrane so no action
potentials can be generated.
Typical exam Questions
1. The diagram shows part of a myofibril from skeletal muscle.
Z line thick filament
Z line
thin filament
Z line
Myasthenia
Myasthenia gravis is a disease which causes muscular weakness.
It develops because of an attack by the body’s own immune system
on neuromuscular junctions.
Fig 2 shows a normal neuromuscular junction and one affected by
the disease (myasthenic).
A band
A band
Sarcomere
Sarcomere
Fig 2. Myasthenic neuromuscular junction
Normal
Describe two features, visible in the diagram, which show that
the myofibril is contracted.
Vesicles
containing
acetylcholine
2. Explain the role of calcium ions in bringing about contraction
of a muscle fibre.
3. Explain the role of ATP in bringing about contraction of a
muscle fibre.
Myasthenic
Axon of motor
neurone
Acetylcholine
receptors
Answers
1. H band not visible/reduced / little/no thick filament/myosin
only region / ends of thin filaments/actin close together;
I band not visible/reduced / little/no thin filament/actin only
region;
A band occupies nearly all sarcomere / thick filament/myosin
close to Z line;
Large zone of thick-thin overlap;
Acetylcholinesterase
Membrane of
muscle cell
How does the myasthenic junction affect transmission across the
junction?
• The myasthenic junction has fewer folds/ fewer receptors, so
there are fewer Na + channels open and less chance of
depolarization
2. Bind to troponin;
Remove blocking action of tropomyosin / expose myosin
binding sites;
3. Allows myosin to detach from actin / to break cross bridge;
[allow attach and detach]
Releases energy to recock/swivel/activate myosin head;
2
•
The synaptic cleft is wider than normal so it takes longer for the
neurotransmitter to diffuse across.
•
There is a different ratio of receptors to esterase so the
neurotransmitter is more likely to be destroyed before binding
to the receptor
•
Acetylcholinesterase is in shallower folds/more exposed so
there is more chance that the transmitter will be destroyed before
it binds to the receptor
Bio Factsheet
190. Neuromuscular Junctions
www.curriculum-press.co.uk
Practice Questions
3. The diagram shows a normal neuromuscular junction and one
affected by the disease (myasthenic).
1. The diagram shows the structure of a neuromuscular junction.
Identify structures A-G
Myasthenic
Normal
Vesicles
containing
acetylcholine
A
Axon of motor
neurone
B
Acetylcholine
receptors
C
F
D
E
Acetylcholinesterase
Membrane of
muscle cell
The changes in the neuromuscular junctions in myasthenia
gravis result in fewer calcium ions entering muscle fibres.
Explain how this reduces interactions between actin and
myosin filaments and, thus, the strength of muscle contractions.
G
2. Give two differences between a cholinergic synapse (one where
the neurotransmitter is acetylcholine) and a neuromuscular
junction.
4. The bacterium Clostridium botulinum releases botulinum toxin
which binds to presynaptic membranes of neuromuscular
junctions, blocking the release of acetylcholine. Death from
botulism may occur due to paralysis of the breathing system.
Explain how the action of the botulinum toxin could cause
paralysis of the breathing system.
4. acetylcholine does not bind to receptors;
on postsynaptic membrane / motor end plate membrane/sacrolemma;
depolarization/action potential does not occur;
intercostal/diaphragm muscles (do not contract);
3. tropomyosin on actin;
calcium ions needed to move it out of the way;
allows myosin to bind to actin/formation of cross bridges;
fewer calcium ions leads to fewer power strokes/
ratchet actions;
needed for activation of ATPase;
2. neurone to neurone and neurone to muscle;
action potential in neurone and no action potential in muscle/sarcolemma;
no summation in muscle;
muscle response always excitatory (never inhibitory);
some neuromuscular junctions have different neurotransmitters;
1. A
B
C
D
E
F
G
Myelin sheath
Motor neurone
Mitochondria
Synaptic bulb
Synaptic vesicles (containing neurotransmitter)
Presynaptic membrane
Postsynaptic membrane (sarcolemma)
Answers
Acknowledgements:
This Factsheet was researched and written by Kevin Byrne.
Curriculum Press, Bank House, 105 King Street, Wellington, Shropshire, TF1 1NU.
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