Test
NMS Set 3 Quiz - NMJ's, NMJ pharmacology and muscles.
Preguntas del test (36)
1What two receptor types are found in abundance on the post synaptic membrane found at the NMJ?
- AVoltage gated sodium
- BnAchR
- CVoltage gated calcium
- DNMDA
2What is the correct process of synaptic transmission?
- AAction 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.
- BCa2+ entry -> Action potential produced -> Ach vesicles fuse with the pre-synaptic membrane.
3When Ach binds to the post-synaptic membrane, the resting membrane potential of the muscle cell goes from -90mV to...
- A-20mV
- B+10mV
- C0mV
- D-55mV
4Binding of Ach causes production of an end plate potential. How does this end plate potential permit the subsequent initiation of an action potential?
- AThe EPP causes voltage gated sodium channels to open which leads to an action potential being produced in the muscle cell.
- BThe EPP causes voltage gated chloride channels to close which leads to an action potential being produced in the muscle cell.
5Acetylcholine is recycled from the synaptic cleft as what two components?
- AAcetate
- BCholine
- CChlorine
- DAcetyl
6What enzyme reincorporates the two components of Ach back into Ach?
- ACholineacetyltransferase
- BAcetylcholinetransferase
- CAcetylcholinesterase
7After the initiation of an end plate potential and subsequent action potential, how does this action potential resulting in calcium efflux from the sarcoplasmic reticulum?
- AThe 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.
- BThe 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.
8What is the function of the light chain of botulinum toxin?
- AThe 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.
- BThe 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.
9What is the function of the heavy chain of botulinum toxin?
- AThe 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.
- BThe 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.
10Very active muscle fibres are amongst the first to be affected by botulinum toxin.
- AVerdadero
- BFalso
11Name a depolarising blocker of the NMJ
- ATubocurarine
- BPancuronium
- CSuxamethonium
- DHexamethonium
12Give two examples of non-depolarising neuromuscular junction blockers
- ATubocurarine
- BPancuronium
- CSuxamethonium
- DHexamethonium
13Anti-cholinesterases can cause suxamethonium-like properties in the synaptic cleft.
- AVerdadero
- BFalso
14What are anti-cholinesterases used for treatment of myasthenia gravis?
- AAuto-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.
- BAuto-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.
15Although 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.
- AVerdadero
- BFalso
16Suxamethonium leads to paralysis because the sustained depolarisation that it causes eventually leads to inactivation of VG Na+ channels.
- AVerdadero
- BFalso
17Myosin heads have GTPase activity that can hydrolyse GTP to recock the myosin head.
- AVerdadero
- BFalso
18What are the three main energy systems of muscle contraction?
- APhosphocreatine
- BLactic acid
- COxidative phosphorylation
- DSubstrate level phosphorylation
- EGlycogenolysis
19Slow twitch fibres mostly take part in anaerobic respiration.
- AVerdadero
- BFalso
20Phosphocreatine is broken down to get inorganic phosphate that can be used in ATP that partakes in muscle contraction.
- AVerdadero
- BFalso
21Pumping of Ca2+back into the sarcoplasmic reticulum to aid in relaxation of the muscle fibre requires ATP.
- AVerdadero
- BFalso
22A motor unit is...
- AA motor neurone that innervates severe muscle cell sarcomeres to produce co-ordinated responses
- BA group of motor neurones that innervate a single muscle cell each to produce co-ordinated responses
23If there is a large force required for a muscle to carry out a task, would slow twitch or fast twitch fibres be used?
- AFast twitch
- BSlow twitch
24Recruitment of motor units describes what?
- AIncreasing the number of motor units firing
- BIncrease the frequency of motor units firing
25Rate coding of motor units describes what?
- AIncreasing the number of motor units firing
- BIncreasing the frequency of motor units firing
26Name some examples of neurogenic motor unit disease
- AGuillain-Barre syndrome
- BALS
- CDuchenne muscular dystrophy
- DDermatomyositis
27Name some examples of myopathic motor unit diseases
- AGuillain-Barre syndrome
- BALS
- CDermatomyositis
- DDuchenne muscular dystrophy
28Most treatment for ALS (motor neurone disease) is symptomatic.
- AVerdadero
- BFalso
29ALS affects what part of the motor system?
- AUpper motor neurones
- BLower motor neurones
- CSensory neurones
30What symptoms can ALS present?
- AWeakness
- BWasting
- CFasciculation
- DCognitive decline
31Guillain-Barre syndrome affects what aspects of the motor system?
- AUpper motor neurones
- BLower motor neurones
- CSensory neurones
- DPeripheral motor neurones
32Guillain-Barre is due to cross-reacting antibodies that attack peripheral nerves.
- AVerdadero
- BFalso
33How could you treat Guillain-Barre?
- APlasma exchange to get rid of cross-reacting antibodies
- BIntravenous immunoglobulin to try to get rid of cross-reacting antibodies
- CIntraneurone injection to stimulate nerve regrowth
34What is responsible for DMD?
- AThe dystrophin protein which anchors intracellular actin to the muscle membrane.
- BA mutation in the dystrophin protein which leads to failed anchorage of intracellular actin to the muscle membrane.
35DMD leads to muscle wasting and weakness.
- AVerdadero
- BFalso
36Serum creatine kinase levels are an indicator of muscle damage in DMD.
- AVerdadero
- BFalso
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