Brainscape's Knowledge GenomeTM

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


See full index

MED221A/B Lectures > MSK 16 - Skeletal muscle physiology > Flashcards

MSK 16 - Skeletal muscle physiology Flashcards

1
Q

what does a motor unit consist of

A

single alpha motor neuron and all the muscle fibres it innervates

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

if the muscle is for fine control would the alpha motor neuron innervate many or few fibres

A

few fibres

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

how many motor units and alpha motor neurons normally supply one muscle

A

many

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

the force of contraction is modulated by what factors when considering motor units

A

modulated by the number and characteristics of motor units recruited

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

how do muscles within a motor unit contract relative to each other

why is this

A

in synchrony

excitation in single motor neuron cell causes all muscles it innervates to contract at once

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

are all muscle fibres within a motor unit the same type

A

yes

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

to generate higher force, does the number of motor units recruited need to increase/decrease

A

increase

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

skeletal muscle force is graded by recruitment of __ __ with progressively ___ ___ ___

A

motor units

increasing excitatory input

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

motor units are normally classified by what

A

muscle type

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

what are the two muscle types that a motor unit can be classified as

A

slow - type 1
fast - type 2

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

how does the size principle of motor units ensure efficiency

A

some motor units have different sizes so that they have different properties which creates different resistance to AP propagation and initiation

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

what order are small and large motor units recruited in

why is this

A

small oxidative motor units are recruited first as they have a lower threshold

fewer large glycolytic motor units are recruited last

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

APs are propagated along the alpha motor neurons to reach what

A

the neuromuscular junction

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

where does neuromuscular transmission take place

A

the neuromuscular junction

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

what must take place in order for muscle motor units to be activated

A

neuromuscular transmission

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

what is the structure of the neuromuscular junction both in general of what two structures join together

A

alpha motor neuron’s terminal bouton synapses with the motor endplate on the muscle fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the structure of the motor endplate

A

there is an active zone where there are vesicles filled with acetylcholine and below it is the synaptic cleft

below the synaptic cleft there are clefts in the muscular endplate with acetylcholine receptors at the top

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does the synaptic cleft connect

A

connection between the synaptic nerve and post synaptic muscle fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the neurotransmitter that the NMJ

A

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

is the motor endplate part of the presynaptic nerve or post synaptic muscle fibre

A

its part of the post synaptic muscle fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

at the NMJ what happens to the myelin sheath

A

the motor axon loses its myelin sheath at the terminal region of the presynaptic nerve and branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what cells are the motor neuron nerves covered with and what does this aid in

A

covered in swann cells - myelin sheaths - that helps the AP propagate along the alpha motor neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

each branch of the motor axon makes contact with what structure

A

each branch makes contact with a muscle fibre cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

describe the molecular organisation of the post synaptic folds

A

two distinct domains

crests (close to the motor end plate) = high conc of Ach receptors and Ach receptor clustering proteins rapsyn and utrophin

depths (far from the motor end plate) = high conc of voltage gated Na+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the two Ach R clustering proteins

A

rapsyn

utrophin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what do the voltage gated Na+ channels do in the depths of the post synaptic membrane

A

AP is propagated along surface of muscle fibre by voltage gated Na+ channels

27
Q

what happens at the NMJ in terms of the pre synaptic events - 3 steps starting from AP

A

AP in presynaptic cell reaches nerve terminal

depolarization opens voltage gated Ca2+ channels leading to Ca2+ influx

increased Ca2+ conc triggers exocytosis of vesicles and release of ACh from vesicles into the synaptic cleft

28
Q

how do the vesicles release ACh and where do they do this

A

vesicles membrane fuse with pre synaptic membrane and pumps out the neurotransmitter

do this at the active zone

29
Q

what are the steps that the vesicles under go in preparation for ACH unloading - 2 things

A

vesicles filled and form vesicle clusters

filled vesicles dock at active zone and undergo priming ready for Ca2+ triggered fusion pore opening

30
Q

what happens once the vesicles have unloaded their ACh contents - 3 options

A

local reuse

fast recycling at the area

clathrin mediated endocytosis and recycling via endosomes where vesicles are filled with ACh

31
Q

what prevents the presynaptic terminal from enlarging from vesicle binding

A

vesicles undergo endocytosis and are recycled

32
Q

AChRs are examples of what kind of channels

A

directly/ligand gated ion channels

33
Q

on the post synaptic cells how many subunits are there on the Ach receptor

A

5 subunits

34
Q

which of the subunits on the ACh receptor are Ach receptors

A

the 2 alpha subunits

35
Q

what opens the channels on the ACh receptor

A

when receptor has 2 molecules bound the channels open

36
Q

what happens after the ACh receptor channels open

A

movement of ions across the membrane causes a current - the end plate current

37
Q

what two ions are involved in generating the end plate current at the ACh receptor

A

Na+ and K+

38
Q

how do Na+ and K+ contribute to the end plate t

A

Na+ is high conc in extracellular fluid and low in intracellular fluid (cytosol of muscle fibres)

K+ is high conc in intracellular fluid and low in extracellular fluid

when channels on AChR opens both Na+ and K+ move down their concentration gradient and depolarises the region

39
Q

what happens to the Na+ K+ movement once the end plate current depolarisation has begun

A

as it depolarises you get less Na+ and K+ movement into region as the conc gradient is decreasing

40
Q

what are the post synaptic events at the NMJ - 4 things

A

2ACh binds at transmitter gated channels

channel opens leading to Na+ inflow and K+ outflow

motor end plate is locally depolarised by current

voltage gated Na+ channels open causing Na+ inflow which depolarises the area and propagates muscle AP

41
Q

the end plate current and end plate potential are terminated by what and how does this happen

A

terminated by ACh-esterase in the synaptic cleft

does so by creating unbinding of Ach at the AChR binding which reduces ACh concentration in the synaptic cleft

42
Q

where is the enzyme Achetylcholinesterase located

what structures does it hold together

A

anchored to the collagen fibrils of the basement membranes

holds the presynaptic nerve and muscle end plate together

43
Q

what does AchE do to ACh

A

hydrolyses it

ACh + H2O -> choline and acetate

44
Q

what happens to the components of ACh after its been hydrolyzed by AChE

A

choline diffuses back into the presynaptic terminal and is reabsorbed and loaded back into vesicles

45
Q

AChE is the physiological target of which substances

A

insecticides and military nerve gases

46
Q

what are the two types of neurological blockades which are used during surgery

A

depolarising

non-depolarising

47
Q

depolarising neurological blockades have what sort of a relationship with AChR and AChE

A

AChR agonist

not broken down by ACh-esterase

48
Q

Non depolarising neurological blockades have what sort of a relationship with AChR and channels

A

AChR antagonist

binds but doesnt open channels

49
Q

what do agonists do and what do antagonists do to receptors

A

agonists = activate receptor and allows for intracellular response

antagonist = blocks receptors and prevents process and response

50
Q

what are alpha toxins

A

specific blockers of nicotinic AChRs

51
Q

what is the specific type of channel are the AChRs at the post synaptic cell

A

nicotinic ACh-gated ion channel

52
Q

the end plate current causes a change in what

A

in membrane potential

53
Q

the current increases above threshold and what event follows

A

AP is automatically fired

54
Q

what happens to the end plate current when a alpha toxin is applied

A

the membrane potential does not exceed threshold - thus the AP is not fired

55
Q

the end plate potential is always ____ in vivo

A

supra-threshold

56
Q

how far can end plate potentials travel

why is this

A

short distances

EPPs arent propagated like nerve/muscle APs, they are just localised change of potential due to ACh only being in that one place on the muscle fibre

57
Q

what is the duration of end plate potential determined by

A

the mean open time of all AChRs at the synapse

ie how long the AChRs stay open which in turn is determined by the AChE activity

58
Q

what are 3 examples of abnormal pre-synaptic transmissions

A

lambert eaten syndrome

diabetes

naturally occuring toxins like botox

59
Q

what are 4 examples of abnormal post-synaptic transmissions

A

alpha toxins

anti-AChE

organophosphates that prevent AChE breakdown

depolarising (ACh agonists) or non depolarizing drugs (ACh Antagonists)

60
Q

do alpha toxins affect the pre or post synaptic neuromuscular transmission

A

post

61
Q

what is the most common primary disorder of the NMT

A

myasthenia gravis

62
Q

what is myasthenia gravis and what are its symptoms

A

autoimmune disease resulting in fewer AChRs

causes weakness and fatigability of voluntary muscles especially facial muscles

63
Q

how can myasthenia gravis be treated (to some extent)

how does this work

A

AChE inhibitors which would prolong the activity of ACh at the NMJ

64
Q

what is the consequence of having fewer AChRs due to myasthenia gravis

A

may not get every AP in the nerve depolarising motor end plate regions sufficiently to open the voltage gated Na+ channels on the post synaptic membrane

MED221A/B Lectures (23 decks)

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