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Y1 - ICPP > Lecture 10 - Neuromuscular > Flashcards

Lecture 10 - Neuromuscular Flashcards

1
Q

What structure passes a signal from a motor neurone to a muscle?

A

Neuromuscular junction

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2
Q

What stimulates the release of neurotransmitter into the synaptic cleft of the neuromuscular junction?

A

Ca2+

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3
Q

How does Ca2+ influx causing neurotransmitter release occur?

A

Depolarisation stimulates Voltage Gated Ca2+ Channels to open

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4
Q

What generally happens at the nerve terminal once action potential reaches it?

A

VG Ca2+ channels open
Ca2+ influx
Increased [Ca2+]
ACh (Neurotransmitter) released into synaptic cleft

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5
Q

How does an increased frequency in action potentials to a nerve terminal affect terminal Ca2+ influx and therefore neurotransmitter release?

A

Increased amount of Ca2+ influx
MORE Neurotransmitter released

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6
Q

What is the structure of a Voltage-gated Ca2+ channel similar to?

A

Voltage gated Na+ channel

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7
Q

What is the structure of a voltage gated Ca2+ channel?

A

1 alpha sub unit made up of 4 repeats
Charged amino acids on repeats I and IV

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8
Q

What is a common Ca2+ channel?

A

L Type voltages gated Ca2+ channels

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9
Q

What family of drugs are used to block L-Type Ca2+ channels?

A

DHP (Dihydropyridines)

E.g Nifedipine

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10
Q

What is the significance of other subunits associating with Na+ channels or Ca2+ channels?

A

Fine tunes the properties
Ensures it carries out set function

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11
Q

What can the post synaptic membrane of a neuromuscular junction be called?

A

End plate

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12
Q

What receptors are present of the end plate/post synaptic membrane at a neuromuscular junction?

A

nACHR (Nicotinic Aceytlcholine receptors)

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13
Q

Once Ca2+ influx to axon terminal at a neuromuscular junction has occured, what happens? How does the neurotransmitter get released into the cleft?

A

Ca2+ binds to synaptotagmin
Vesicle bought close to membrane
Snare complex make a fusion pore
Transmitter released through this pore

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14
Q

Where is synaptotagmin?

A

On vesicle membrane

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15
Q

Where is the snare complex?

A

On the presynaptic membrane

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16
Q

How many ACh need to bind to the nACHR on the skeletal muscle membrane?

A

2 to each nAChR

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17
Q

What is the selectivity of nicotinic Acetylcholine receptors like?

A

Not very specific
Allows cations to move through
Na+ and Ca2+ in
K+ out

18
Q

What type of channel are nAChR?

A

Ligand gated ion channels

19
Q

What happens when ACh binds to the AChR on the muscle membrane (end plate)?

A

Na+ influx into muscle causing depolarisation
If threshold potential reached Action potential in smooth muscle will be fired

20
Q

What is the depolarisation that occurs before an action potential occurs in the end plate (muscle) at a neuromuscular junction?

A

End plate potential

21
Q

How does amount of Ca2+ entry into axon terminal effect end plate potential?

A

Less Ca2+ in terminal = less neurotransmitter released = less nAChR opened = less Na+ into end plate = LOWER AMPLITUDE End plate potential

22
Q

What is the problem with lower amplitude end plate potentials at a neuromuscular junction?

A

Unlikely to depolarise enough to reach threshold potential for an action potential

23
Q

What is the enzyme that breaks down the ACh on the Na+ ligand gated ion channels (nAChR) on the end plate/postsynaptic membrane?

A

Aceytlcholine esterase
ACh esterase

24
Q

What is the effect of blocking nicotinic ACh receptors at neuromuscular junctions?

A

Paralysis since action potentials cannot be fired due to prevention of depolarisation (no Na+ influx)

25
Q

What are the 2 types of blockers of nACh receptors?

A

Competitive blockers
Non competitive blockers

26
Q

What is an example of a competitive nAChR blocker?

A

d-tubocurarine (d-TC)

27
Q

What is the mode of action of d-TC (d-tubocurarine)?

A

Competes with ACh for the binding site of the nAChR (Ligand gated Na+ channel)

28
Q

What happens with the competitive blocker d-tubocurarine (d-TC) when ACh concentration is very high?

A

ACh may outcompete d-TC so its effects are minimal

29
Q

How does the nAChR blocker succinylcholine work?

A

Activates nAChR maintaining depolarisation causing the nACh channels to inactivate

30
Q

In surgery what is important to accompany a neuromuscular blocker and why?

A

Neuromuscular blocker = paralysis

Anaesthetic = to not feel pain

A patient who has only had a neuromuscular blocker wont be able to move but will be able to feel the pain

31
Q

What is Mayasthenia gravis?

A

Autoimmune disease targeting nACh receptors

32
Q

What effect does Mayasthenia gravis have on the end plate at a neuromuscular junction?

A

Damages the nAChR reducing number of functional channels

More ACh needed to reach threshold potential

33
Q

What effect does Mayasthenia gravis have on muscles and why?

A

Profound weakness

Due to endplate potentials being reduced in amplitude
Means threshold potentials often not reached

34
Q

How can Myasthenia gravis be diagnosed?

A

Inhibit the ACh esterase enzyme so the ACh is not quickly broken down and can accumulate
And then see if the muscle strength increases (more Ligand gated Na+ channels open so more likely that end plate potential reaches threshold)

35
Q

What is the test called to diagnose myasthenia gravis?

A

Edrophonium test

Sees if facial muscle weakness improved by the ACh esterase inhibitor edrophonium chloride

36
Q

How is organophosphate poisoning bad?

A

Permanently inhibit ACh esterase

37
Q

Where are muscarinic Acetylcholine receptors located?

A

Following postganglionic parasympathetic neurones on the target tissues

38
Q

How does the type of synaptic transmission differ between nAChRs and mAChRs?

A

nAChR = fast synaptic transmission

mAChR = slow synaptic transmission

39
Q

Why is nAChR fast synaptic transmission?

A

The receptor and ion channel are the same protein
It is a ligand gated ion channel so depolarisation is fast

40
Q

Why is mAChR slow synaptic transmission?

A

mAChR is a G protein coupled receptor

Receptor and ion channel are separate proteins

G protein needs to be activated triggering a cascade of events in the cell leading to the opening of the ion channel

Y1 - ICPP (23 decks)

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