B io Factsheet

www.curriculum-press.co.uk 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
Presynaptic membrane
(containing neurotransmitter)
Synaptic cleft

Cytoplasm of
muscle fibre

Postsynaptic Myofibril
membrane
(sarcolemma)

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. 13 Troponin moves tropomyosin.
2 Ca2+ channels on the presynaptic membrane open. • Many candidates believe that it is the calcium that moves
3 There is an Influx of Ca2+2 ions from the synaptic cleft into the tropomyosin – it isn’t
synaptic bulb. 14 This exposes myosin binding sites on actin molecules / thin
4 Vesicles move towards presynaptic membrane. filaments
5 Vesicles fuse with presynaptic membrane. 15 The calcium ions activate myosin which releases ATPase to
6 Neurotransmitter e.g. acetylcholine is released from the vesicles. split ATP from mitochondria into ADP and Pi
7 The neurotransmitter diffuses across the gap or synaptic cleft. 16 This energy is used to move the heads of the myosin filaments
8 The neurotransmitter binds to protein receptors on the towards the now exposed binding sites on actin
sarcolemma (post-synaptic membrane)which has a large surface 17 The myosin head binds to the binding site on actin and cross
area for this purpose. bridges are formed
9 The binding of the neurotransmitter to the receptors on the 18 The myosin heads tilt pulling the actin filaments past them
sarcolemma causes sodium channels to open causing an influx 19 As they slide, the heads detach from one site and bind to the
of sodium ions. next in a ratchet mechanism
10 An action potential is generated and there is depolarization 20 As actin filaments from either end of the sarcomere move
along the surface of the muscle/depolarisation spreads down towards each other, the muscle fibre contracts/ there is greater
transverse tubules. overlap between thick and thin filaments
11 Calcium channels in the sarcoplasmic reticulum open. 21 The sarcomere shortens / the distance between Z discs
12 Calcium ions diffuse out and bind to troponin. decreases

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Applying this knowledge

Extract from Chief Examiner's Reports Once you have learned and understood these basic facts, you
What candidates get wrong on this first part should be ready to tackle questions which ask you to apply this
• Many candidates stated that vesicles move across the cleft knowledge.
• Ion movement was often poorly described, with the direction
of movement often omitted. Many candidates incorrectly The cobra is a very poisonous snake.
referred to movement of chlorine or sodium ions at the The molecular structure of cobra toxin
presynaptic knob is similar to the molecular structure of
• Many candidates failed to mention binding to receptors on acetylcholine. The toxin permanently
the postsynaptic membrane prevents muscle contraction.
• Some made reference to depolarisation of the neurone rather
than the membrane

How?
Because the toxin is structurally similar to acetylcholine, it competes
Typical exam Questions for and blocks the acetylcholine receptors. This means that
1. The diagram shows part of a myofibril from skeletal muscle. acetylcholine cannot depolarise the membrane so no action
potentials can be generated.
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 Fig 2. Myasthenic neuromuscular junction

Sarcomere Sarcomere

Describe two features, visible in the diagram, which show that Normal Myasthenic
the myofibril is contracted. Vesicles
containing
2. Explain the role of calcium ions in bringing about contraction Axon of motor
acetylcholine
of a muscle fibre. neurone

3. Explain the role of ATP in bringing about contraction of a Acetylcholine

muscle fibre. 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 Membrane of
region; Acetylcholinesterase muscle cell
A band occupies nearly all sarcomere / thick filament/myosin
close to Z line;
Large zone of thick-thin overlap; How does the myasthenic junction affect transmission across the
junction?
2. Bind to troponin; • The myasthenic junction has fewer folds/ fewer receptors, so
Remove blocking action of tropomyosin / expose myosin there are fewer Na + channels open and less chance of
binding sites; depolarization
3. Allows myosin to detach from actin / to break cross bridge; • The synaptic cleft is wider than normal so it takes longer for the
[allow attach and detach] neurotransmitter to diffuse across.
Releases energy to recock/swivel/activate myosin head;
• 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

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Practice Questions
1. The diagram shows the structure of a neuromuscular junction. 3. The diagram shows a normal neuromuscular junction and one
Identify structures A-G affected by the disease (myasthenic).
Myasthenic
Normal
Vesicles
A containing
Axon of motor
acetylcholine
neurone
B
Acetylcholine
receptors
C
D

F E
Membrane of
Acetylcholinesterase muscle cell

The changes in the neuromuscular junctions in myasthenia

G 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.

2. Give two differences between a cholinergic synapse (one where 4. The bacterium Clostridium botulinum releases botulinum toxin
the neurotransmitter is acetylcholine) and a neuromuscular which binds to presynaptic membranes of neuromuscular
junction. 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.

intercostal/diaphragm muscles (do not contract);

depolarization/action potential does not occur;
on postsynaptic membrane / motor end plate membrane/sacrolemma;
4. acetylcholine does not bind to receptors;

needed for activation of ATPase;

ratchet actions;
fewer calcium ions leads to fewer power strokes/
allows myosin to bind to actin/formation of cross bridges;
calcium ions needed to move it out of the way;
3. tropomyosin on actin;

some neuromuscular junctions have different neurotransmitters;

muscle response always excitatory (never inhibitory);
no summation in muscle;
action potential in neurone and no action potential in muscle/sarcolemma;
2. neurone to neurone and neurone to muscle;

Postsynaptic membrane (sarcolemma) G

Presynaptic membrane F
Synaptic vesicles (containing neurotransmitter) E
Synaptic bulb D
Mitochondria C
Motor neurone B
Myelin sheath 1. A
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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