Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SFI Test 1 > Neuromuscular Junction > Flashcards

Neuromuscular Junction Flashcards

1
Q

What is a motor unit?

A

One motor neuron innervates one group of muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens to cause an action potential in the muscle fiber?

A

Motor neuron releases ACh

AChRs allow influx of Na and efflux of K

Leads to activation of v-g Na channels and action potential propagation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the end-plate current?

A

Entrance of Sodium ions into the muscle fiber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the end-plate potential?

A

The change in muscle fiber potential, more than enough to produce a postsynaptic action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are miniature end plate potentials?

A

Like EPPs, but much smaller in amplitude

Caused by spontaneous release of quanta of ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the safety factor?

A

Difference between the actual EPP and threshold potential required to generate muscle action potential

EPP is more positive than threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the structure of a nicotinic AChR?

A

5 subunits arranged around a central pore

2 a, 1 B, y, and delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is characteristic of an embryonic AChR?

A

Longer single channel mean open time and lower single channel current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is characteristic of an adult AChR?

A

Shorter single channel mean open time and greater single channel current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does the motor neuron know where to form synapses?

A

Motor neuron releases ACh before making contact

Muscle membrane responds to ACh before contact

Synapses form where these interactions take place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are AChRs located before innervation?

A

Aggregate in center of developing muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does the nerve induce increased clustering of receptors?

A

Preexisting receptors are redistributed

New receptors are synthesized

Turnover is decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of agrin?

A

Released by the nerve

Initiates AChR clustering by regulating the interaction of MuSK and LRP4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the function of Dok-7?

A

Required to activate MuSK after binding of agrin and thus aggregate AChRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of rapsyn?

A

Binds to AChRs and aggregates them to synapses

Other components of NMJ co-cluster with AChRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What occurs after innervation?

A

Receptor half-life increases, embryonic receptors disappear and adult receptors appear

17
Q

How are excess innervations by other motor neurons eliminated in the developing NMJs?

A

In neuron that will be eliminated, number of receptors on muscle is reduced –> decrease in synaptic strength causes further loss of receptors –> cycle eventually leads to terminal withdrawal

18
Q

What is the function of botulinum toxin?

A

Blocks ACh release

19
Q

What is the function of curare and bungarotoxin (snake venom)?

A

Inhibits AChRs

20
Q

What is the function of physostigmine and neostigmine?

A

Inhibits AChE

21
Q

What is the function of tetrodotoxin?

A

Blocks Muscle Na channels

22
Q

What is the function of Conotoxins?

A

Block neuronal Ca channels, muscle Na channels, and AChRs

23
Q

Describe Myasthenia gravis

A

Most patients have antibodies against AChRs, some to MuSK

Causes reduced AChRs at NMJ

EPPs and MEPPs are smaller than normal

24
Q

What are the clinical features of Myasthenia gravis?

A

Weakness and fatigue of voluntary muscles

Worsens on exertion

Ocular muscle weakness

25
Q

What are the treatments for MG?

A

AChE inhibitors

Drugs to reduce immune response

Removal of AChR antibodies

26
Q

Describe Lambert-Eaton syndrome.

A

Antibodies against presynaptic Ca channels

Affects primarily limb muscles

Exercise improves weakness

27
Q

What are the congenital myasthenic syndromes?

A

AChRs

Dok7

MuSK

rapsyn

LRP4

28
Q

Describe botulism

A

Caused by Clostridium botulinum

Affects autonomic nervous system as well as NMJ

Death can occur from respiratory muscle paralysis

29
Q

What is botulinum toxin used to treat?

A

Muscle contractures and spasms, strabismus (cross-eyes) and headaches

30
Q

How does ageing affect the NMJ?

A

NMJ becomes unstable over time

Synaptic area decreases as AChRs fragment and number of postsynaptic folds decreases

Eventually lose motor nerves

Reinnervation is less likely to occur

SFI Test 1 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions