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...
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.
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.
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.
Question 16
Question
Suxamethonium leads to paralysis because the sustained depolarisation that it causes eventually leads to inactivation of VG Na+ channels.
Question 17
Question
Myosin heads have GTPase activity that can hydrolyse GTP to recock the myosin head.
Question 18
Question
What are the three main energy systems of muscle contraction?
Question 19
Question
Slow twitch fibres mostly take part in anaerobic respiration.
Question 20
Question
Phosphocreatine is broken down to get inorganic phosphate that can be used in ATP that partakes in muscle contraction.
Question 21
Question
Pumping of Ca2+back into the sarcoplasmic reticulum to aid in relaxation of the muscle fibre requires ATP.
Question 22
Question
A motor unit is...
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?
Question 24
Question
Recruitment of motor units describes what?
Question 25
Question
Rate coding of motor units describes what?
Question 26
Question
Name some examples of neurogenic motor unit disease
Question 27
Question
Name some examples of myopathic motor unit diseases
Question 28
Question
Most treatment for ALS (motor neurone disease) is symptomatic.
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?
Question 32
Question
Guillain-Barre is due to cross-reacting antibodies that attack peripheral nerves.
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?
Question 35
Question
DMD leads to muscle wasting and weakness.
Question 36
Question
Serum creatine kinase levels are an indicator of muscle damage in DMD.