Synaptic Transmission And Neuromuscular Junction (session 5) Flashcards Preview

Semester 1-ICPP > Synaptic Transmission And Neuromuscular Junction (session 5) > Flashcards

Flashcards in Synaptic Transmission And Neuromuscular Junction (session 5) Deck (26):
1

How is a signal passed from nerve to muscle?

Neuromuscular junction (synapse between nerve and skeletal muscle fibre)

2

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

Na+
K+
Ca2+

3

What happens at the nerve terminal? (4)

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

4

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

Because the concentration of Ca2+ inside is so low

5

Complete the sentence:

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

Increases

6

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

Na+

7

What is a pore forming subunit necessary for?

A functional channel

8

What do other associated subunits do in channels?

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

9

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

FALSE

10

What does acetylcholine esterase do?

Breaks down ACh

11

What type of acetylcholine receptors are on the postsynaptic membrane?

Nicotinic

12

Describe the process of transmitter release (5)

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

13

What is reverse potential?

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

14

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

Leads to a conformational change and the pore opens

15

What is excitation contraction coupling?

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

16

Give an example of a competitive nicotinic ACh receptor blocker

Tubocurarine

17

Give an example of a depolarising nicotinic ACh receptor blocker

Succinylcholine

18

How can the block by d-tubocurarine be overcome?

By increasing the concentration of ACh

19

What is a potential problem of using succinylcholine during operations?

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

20

Name an autoimmune disease targeting nACh receptors

Myasthenia gravis

21

What happens in myasthenia gravis?

Patients suffer profound weakness
Weakness increases with exercise

22

What causes myasthenia gravis?

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

Complete the sentence:

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

Nicotinic
End-plate potential

24

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

Due to excitation-contraction coupling

25

What is the difference between nicotinic and muscarinic receptors?

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

26

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

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