ICPP - Electrical Excitability Flashcards

1
Q

What is a neuromuscular junction?

A

The synapse between a nerve and a skeletal muscle fibre.

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2
Q

What role does Ca2+ play at the nerve terminal?

A

Depolarisation opens the voltage-gates Ca2+ channels, leading to Ca2+ entry. This increases the intracellular Ca2+ concentration, leading to neurotransmitter release from the vesicles.

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3
Q

How is increase in frequency of action potentials linked with amount of neurotransmitter released?

A

More action potentials = increase in intracellular [Ca2+] = more transmitter released.

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4
Q

What is the purpose of the other associated subunits attached to the alpha subunit in the Ca2+ channel?

A

Fine-tunes properties and enables correct regulation of channel activity

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5
Q

Which activates faster - Ca2+ or Na2+ channels?

A

Na2+ channels are much faster than Ca2+ channels.

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6
Q

How can snail neurones be used to show that Ca2+ is responsible for Ca2+ channel inactivation?

A

Snails have Ba2+ as well, which will pass through Ca2+ channels instead of Ca2+. When it does this, much less inactivation of channels is seen, so it must be increased intracellular [Ca2+] that leads to inactivation of Ca2+ channels

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7
Q

What are motor end plates?

A

The point at which the axon connects to the myofibres

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8
Q

What are snare proteins?

A

These form snare complexes are direct neurontransmitter to be released. They do this by bringing the vesicles close to the membrane and forming a “fusion pore”, through which neurotransmitter is released.

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9
Q

How many molecules of ACh must bind to nicotinic ACh receptors to make them open?

A

2

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10
Q

Which ions are allowed through nACh receptors?

A

Na+ is allowed in, and K+ is allowed out.

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11
Q

What happens to a muscle action potential once it reaches an end plate?

A

It is initiated adjacent to the end-plate and propagates along the muscle fibre, initiating contraction of the skeletal muscle fibre.

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12
Q

What are the two types of blockers of nicotinic ACh receptors?

A

Competitive blockers eg tubocurarine, and depolarising blockers eg succinylcholine

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13
Q

How can competitive blocking be overcome?

A

Increase the concentration of ACh.

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14
Q

How does a depolarising block work?

A

Channels become depolarised by blocker, meaning that they cannot be depolarised by ACh.

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15
Q

What is myasthenia gravis?

A

Autoimmune disease where antibodies lead to loss of functional nAChR by complement mediated lysis and receptor degradation.

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16
Q

What are the symptoms of myasthenia gravis?

A

Endplate potentials are reduced in amplitude leading to muscle weakness and fatigue which worsens with exercise.

17
Q

What is the difference in response times of nAChR and mAChR?

A

Nicotinic AChR produce a fast depolarisation because they are ligand gated. mAChR produce a slower cascade response because they are coupled to G-proteins which are slower to respond.