Synaptic Transmission And Neuromuscular Junction (session 5) Flashcards

1
Q

How is a signal passed from nerve to muscle?

A

Neuromuscular junction (synapse between nerve and skeletal muscle fibre)

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2
Q

Which voltage-gated channels are present in the nerve terminal?

A

Na+
K+
Ca2+

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3
Q

What happens at the nerve terminal? (4)

A
  1. Depolarisation
  2. Opens voltage-gated Ca2+ channels
  3. Ca2+ entry
  4. Release of neurotransmitter
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4
Q

Why can the internal concentration of Ca2+ be increased significantly at the nerve terminal?

A

Because the concentration of Ca2+ inside is so low

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5
Q

Complete the sentence:

Increasing the frequency of AP _________ the amount of nerve terminal Ca2+ entry

A

Increases

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6
Q

The alpha subunit of voltage-gated Ca2+ channels is very similar to which other voltage-gated channel?

A

Na+

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7
Q

What is a pore forming subunit necessary for?

A

A functional channel

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8
Q

What do other associated subunits do in channels?

A

Fine-tune the properties and enable correct regulation of channel activity

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9
Q

True or false: voltage-gated Ca2+ channels activate quicker than voltage-gated Na+ channels

A

FALSE

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10
Q

What does acetylcholine esterase do?

A

Breaks down ACh

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11
Q

What type of acetylcholine receptors are on the postsynaptic membrane?

A

Nicotinic

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12
Q

Describe the process of transmitter release (5)

A
  1. Ca2+ entry through Ca2+ channels
  2. Ca2+ binds to synaptotagmin
  3. Vesicle brought close to membrane
  4. Snare complex make fusion pore
  5. Transmitter released through this pore
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13
Q

What is reverse potential?

A

No net flow of charge when the channel is open-halfway between K+ and Na+ equilibrium potential

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14
Q

What happens at the synaptic cleft when two ACh molecules bind to the receptor?

A

Leads to a conformational change and the pore opens

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15
Q

What is excitation contraction coupling?

A

Muscle AP initiated adjacent to the end-plate and propagates along the muscle fibre.
The AP initiates contraction of the skeletal muscle fibre.

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16
Q

Give an example of a competitive nicotinic ACh receptor blocker

A

Tubocurarine

17
Q

Give an example of a depolarising nicotinic ACh receptor blocker

A

Succinylcholine

18
Q

How can the block by d-tubocurarine be overcome?

A

By increasing the concentration of ACh

19
Q

What is a potential problem of using succinylcholine during operations?

A

Sometimes the anaesthetic doesn’t work but the neuromuscular blocker does work so the patient is left paralysed but can still feel pain

20
Q

Name an autoimmune disease targeting nACh receptors

A

Myasthenia gravis

21
Q

What happens in myasthenia gravis?

A

Patients suffer profound weakness

Weakness increases with exercise

22
Q

What causes myasthenia gravis?

A

Antibodies directed against nACh receptor on postsynaptic membrane of skeletal muscle. Antibodies lead to loss of functional nAChR by complement mediated lysis and receptor degradation. Endplate potentials are reduced in amplitude, leading to muscle weakness and fatigue

23
Q

Complete the sentence:

ACh binds to _________ ACh receptors on the muscle end-plate , causing a depolarisation called the ___-_____ _________

A

Nicotinic

End-plate potential

24
Q

Why does the muscle fibre contract when an AP is initiated there?

A

Due to excitation-contraction coupling

25
Q

What is the difference between nicotinic and muscarinic receptors?

A

Nicotinic receptors are ligand-gated

Muscarinic receptors are in the parasympathetic nervous system so there is no intrinsic ion channel involved

26
Q

Why do muscarinic AChR produce a slower response than nicotinic AChR?

A

mAChR are coupled to G-proteins which trigger a cascade of events in the cell