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NMS Set 3 Quiz - NMJ's, NMJ pharmacology and muscles.

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Question 1

Question
What two receptor types are found in abundance on the post synaptic membrane found at the NMJ?
Answer
  • Voltage gated sodium
  • nAchR
  • Voltage gated calcium
  • NMDA

Question 2

Question
What is the correct process of synaptic transmission?
Answer
  • Action potential received at pre-synaptic terminal -> Ca2+ entry due to VG Ca2+ open -> binds to synaptotagmin -> conformational change -> Ach vesicles fuse with pre-synaptic membrane.
  • Ca2+ entry -> Action potential produced -> Ach vesicles fuse with the pre-synaptic membrane.

Question 3

Question
When Ach binds to the post-synaptic membrane, the resting membrane potential of the muscle cell goes from -90mV to...
Answer
  • -20mV
  • +10mV
  • 0mV
  • -55mV

Question 4

Question
Binding of Ach causes production of an end plate potential. How does this end plate potential permit the subsequent initiation of an action potential?
Answer
  • The EPP causes voltage gated sodium channels to open which leads to an action potential being produced in the muscle cell.
  • The EPP causes voltage gated chloride channels to close which leads to an action potential being produced in the muscle cell.

Question 5

Question
Acetylcholine is recycled from the synaptic cleft as what two components?
Answer
  • Acetate
  • Choline
  • Chlorine
  • Acetyl

Question 6

Question
What enzyme reincorporates the two components of Ach back into Ach?
Answer
  • Cholineacetyltransferase
  • Acetylcholinetransferase
  • Acetylcholinesterase

Question 7

Question
After the initiation of an end plate potential and subsequent action potential, how does this action potential resulting in calcium efflux from the sarcoplasmic reticulum?
Answer
  • The action potential travels down T-tubules. A receptor called the DHP receptor (a voltage sensor) detects this voltage change and undergoes a conformational shape change. This conformational change leads to unplugging of ryanodine from the sarcoplasmic reticulum which allows mass efflux of calcium from the sarcoplasmic reticulum.
  • The action potential travels down T-tubules. A receptor called the DNP receptor (a voltage sensor) detects this voltage change and undergoes a conformational shape change. This conformational change leads to unplugging of ryanodine from the sarcoplasmic reticulum which allows mass efflux of calcium from the sarcoplasmic reticulum.

Question 8

Question
What is the function of the light chain of botulinum toxin?
Answer
  • The light chain binds to the pre-synaptic membrane at the point where neurotransmission is occuring. This causes the botulinum toxin to be up-taken into the pre-synaptic terminal.
  • The light chain is a protease which cleaves proteins that are fundamental for exocytosis of neurotransmitter to occur. This therefore means that exocytosis of neurotransmitter does not occur and the muscle remains paralysed.

Question 9

Question
What is the function of the heavy chain of botulinum toxin?
Answer
  • The heavy chain binds to the pre-synaptic membrane at the point where neurotransmission is occuring. This causes the botulinum toxin to be up-taken into the pre-synaptic terminal.
  • The heavy chain is a protease which cleaves proteins that are fundamental for exocytosis of neurotransmitter to occur. This therefore means that exocytosis of neurotransmitter does not occur and the muscle remains paralysed.

Question 10

Question
Very active muscle fibres are amongst the first to be affected by botulinum toxin.
Answer
  • True
  • False

Question 11

Question
Name a depolarising blocker of the NMJ
Answer
  • Tubocurarine
  • Pancuronium
  • Suxamethonium
  • Hexamethonium

Question 12

Question
Give two examples of non-depolarising neuromuscular junction blockers
Answer
  • Tubocurarine
  • Pancuronium
  • Suxamethonium
  • Hexamethonium

Question 13

Question
Anti-cholinesterases can cause suxamethonium-like properties in the synaptic cleft.
Answer
  • True
  • False

Question 14

Question
What are anti-cholinesterases used for treatment of myasthenia gravis?
Answer
  • Auto-antibodies that bind to nAchR's at NMJ's which are indicated in Myasthenia Gravis compete for the agonist binding site (Ach being the agonist). By using an anti-cholinesterase, you increase the amount of Ach present in the synaptic cleft which can out-compete the auto-antibodies for the nAchR binding site and thus reverse the inhibitory effects.
  • Auto-antibodies that bind to nAchR's at NMJ's which are indicated in Myasthenia Gravis compete for the agonist binding site (Ach being the agonist). By using an anti-cholinesterase, you increase the amount of Ach present in the synaptic cleft which can out-compete the auto-antibodies for the nAchR binding site and thus reverse the excitatory effects.

Question 15

Question
Although suxamethonium is a depolarising NMJ blocker, it is broken down more slower than Ach and therefore sustains depolarisation of the muscle cells, leading to fasciculations.
Answer
  • True
  • False

Question 16

Question
Suxamethonium leads to paralysis because the sustained depolarisation that it causes eventually leads to inactivation of VG Na+ channels.
Answer
  • True
  • False

Question 17

Question
Myosin heads have GTPase activity that can hydrolyse GTP to recock the myosin head.
Answer
  • True
  • False

Question 18

Question
What are the three main energy systems of muscle contraction?
Answer
  • Phosphocreatine
  • Lactic acid
  • Oxidative phosphorylation
  • Substrate level phosphorylation
  • Glycogenolysis

Question 19

Question
Slow twitch fibres mostly take part in anaerobic respiration.
Answer
  • True
  • False

Question 20

Question
Phosphocreatine is broken down to get inorganic phosphate that can be used in ATP that partakes in muscle contraction.
Answer
  • True
  • False

Question 21

Question
Pumping of Ca2+back into the sarcoplasmic reticulum to aid in relaxation of the muscle fibre requires ATP.
Answer
  • True
  • False

Question 22

Question
A motor unit is...
Answer
  • A motor neurone that innervates severe muscle cell sarcomeres to produce co-ordinated responses
  • A group of motor neurones that innervate a single muscle cell each to produce co-ordinated responses

Question 23

Question
If there is a large force required for a muscle to carry out a task, would slow twitch or fast twitch fibres be used?
Answer
  • Fast twitch
  • Slow twitch

Question 24

Question
Recruitment of motor units describes what?
Answer
  • Increasing the number of motor units firing
  • Increase the frequency of motor units firing

Question 25

Question
Rate coding of motor units describes what?
Answer
  • Increasing the number of motor units firing
  • Increasing the frequency of motor units firing

Question 26

Question
Name some examples of neurogenic motor unit disease
Answer
  • Guillain-Barre syndrome
  • ALS
  • Duchenne muscular dystrophy
  • Dermatomyositis

Question 27

Question
Name some examples of myopathic motor unit diseases
Answer
  • Guillain-Barre syndrome
  • ALS
  • Dermatomyositis
  • Duchenne muscular dystrophy

Question 28

Question
Most treatment for ALS (motor neurone disease) is symptomatic.
Answer
  • True
  • False

Question 29

Question
ALS affects what part of the motor system?
Answer
  • Upper motor neurones
  • Lower motor neurones
  • Sensory neurones

Question 30

Question
What symptoms can ALS present?
Answer
  • Weakness
  • Wasting
  • Fasciculation
  • Cognitive decline

Question 31

Question
Guillain-Barre syndrome affects what aspects of the motor system?
Answer
  • Upper motor neurones
  • Lower motor neurones
  • Sensory neurones
  • Peripheral motor neurones

Question 32

Question
Guillain-Barre is due to cross-reacting antibodies that attack peripheral nerves.
Answer
  • True
  • False

Question 33

Question
How could you treat Guillain-Barre?
Answer
  • Plasma exchange to get rid of cross-reacting antibodies
  • Intravenous immunoglobulin to try to get rid of cross-reacting antibodies
  • Intraneurone injection to stimulate nerve regrowth

Question 34

Question
What is responsible for DMD?
Answer
  • The dystrophin protein which anchors intracellular actin to the muscle membrane.
  • A mutation in the dystrophin protein which leads to failed anchorage of intracellular actin to the muscle membrane.

Question 35

Question
DMD leads to muscle wasting and weakness.
Answer
  • True
  • False

Question 36

Question
Serum creatine kinase levels are an indicator of muscle damage in DMD.
Answer
  • True
  • False
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