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CPPS 302 > Class 2 > Flashcards

Class 2 Flashcards

1
Q

During development, all 3 types of muscle originate from where?

A

Somatic mesoderm

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2
Q

What migrates out of the somatic mesodermal germ layer to form muscle fibers

A

Myoblasts

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3
Q

Differentiation of myoblasts into their cell fate and what are believed to be highly correlated?

A

Cell lineage

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4
Q

Coelomic Graft model was used for?

A

To investigate whether muscle type differentiation is determined by myoblast cell lineage, independent of external influences

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5
Q

What is the coelom?

A

Body cavity formed during embryonic development when mesoderm is split into two layers

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6
Q

Satellite cells indicates that cell lineage is not as strong a determinant for what muscle type

A

Skeletal muscle type

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7
Q

Satellite cells are found where?

A

Between the basal lamina and plasma membrane

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8
Q

How are satellite cells activated?

A

After muscle injury or intensive exercise

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9
Q

Satellite cells fuse to what and why?

A

Fuse to themselves to create new muscle fibers or fuse to damaged muscle fibers to repair damage

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10
Q

A satellite cell can transform itself into a muscle fiber of what type?

A

Fast or slow MyHC isoforms

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11
Q

Nerve-evoked electrical activity is an external signal that can (-) muscle phenotype

A

Change

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12
Q

When a nerve from a fast muscle is transplanted into a slow muscle and vice versa —

A

Both re-innervated, muscles change phenotype

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13
Q

Type I motor units, receive (-) amounts of impulses delivered in (-) frequency sequences

A

High, low

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14
Q

Type II motor units, receive (-) amounts of impulses delivered in (-) frequency sequences

A

Low, high

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15
Q

Slow-to-fast muscle phenotype change

A

Difficult, or impossible

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16
Q

Fast-to-slow muscle phenotype change

A

Easy, possible

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17
Q

Why is it difficult to go from slow-to fast muscle phenotype?

A

The amount of background activity will dominate

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18
Q

Depolarization leads to what in muscle?

A

Shortening or mechanical tension

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19
Q

What is possibly more important for muscle activity? Neural or action potential?

A

Neural

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20
Q

Can muscles heal after atrophy?

A

Yes

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21
Q

Changes in muscle usage will lead to what?

A

Changes in muscle phenotype

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22
Q

Factors that can serve as messengers for muscle activity

A
  • Free intracellular Ca
  • Metabolites
  • hypoxia
  • tension
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23
Q

Regulation of force is a question of what?

A

Regulating fiber size

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24
Q

Size can be achieved by regulating three conditions that are?

A
  • number of nuclei
  • rate of protein synthesis
  • rate of protein degradation
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25
Q

Hypertrophy is generally accompanied by:

A

Addition of new nuclei

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26
Q

How are new nuclei created in muscle cells?

A

Satellite cells fusing with pre-existing muscle fiber

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27
Q

What is myostatin?

A

Member of the trans-transforming growth factor B (superfamily)

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28
Q

Myostatin function

A

Role during development where it acts as inhibitor of muscle growth

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29
Q

Disruption of the myostatin gene leads to

A

Development of grossly enlarged muscles, increase in number of fibers and fiber size

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30
Q

Activity is regulated by IGF-binding proteins acting as carriers in blood, or locally binding IGF-I to the extracellular matrix describes what?

A

Insulin-like growth factor I

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31
Q

What organ supplies 75% of circulating IGF-I

A

Liver

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32
Q

What factor has been implicated as a factor promoting hypertrophy

A

IGF-1

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33
Q

IGF-1 function

A
  • increase myotube diameter
  • suppress proteolysis
  • stimulate protein synthesis
  • induce higher number of nuclei
  • promote myoblast synthesis
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34
Q

Hormone for muscles

A

Testosterone

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35
Q

What is the structure where axonal branches of a motor neuron form contact to a group of target muscle fibers within a single motor unit through presynaptic buttons

A

Motor end-plate

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36
Q

There is one somatic motor neuron per (-)

A

One motor unit

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37
Q

Muscles for fine control have (greater, fewer) muscle fibers per motor unit

A

Fewer

38
Q

There are/is (multiple, one) muscle fibers per motor unit

A

Multiple

39
Q

Axonal branches from presynaptic motor neuron form swellings that occupy depression of the muscle fiber are

A

Presynaptic buttons

40
Q

Is there direct contact between presynaptic button and the postsynaptic terminal

A

No

41
Q

Synaptic button that occupies a depression is known as

A

Primary synaptic cleft

42
Q

Sarcolemma of the muscle fiber that forms the infolding deep junctional fold is what?

A

Secondary synaptic cleft

43
Q

What kind of synapse if the neuromuscular junction?

A

Chemical Synapse

44
Q

What separates the presynaptic button and the postsynaptic terminal?

A

Synaptic clefts

45
Q

Synaptic vesicles are derived from the what?

A

Neuronal soma (cell body)

46
Q

What step is: acetylcholine is enclosed by synaptic vesicles and transported by kinesin along the axon by anterograde axonal transport

A

Step 1 in synaptic transmission within the neuromuscular junction of the skeletal muscle

47
Q

What is a neuromuscular junction?

A

A chemical synapse between a motor neuron and a muscle fiber

48
Q

Acetylcholine is enclosed by the membrane-bound (-)

A

Synaptic vesicles

49
Q

Where are synaptic vesicles located where?

A

Presynaptic terminals

50
Q

Molecular motor proteins are what?

A

Kinesin

51
Q

What is the highway of the axon?

A

Microtubule of the axon

52
Q

What step is: depolarization of the axon terminal activates the voltage-gated Ca channels, increase in Ca induces exocytosis of synaptic vesicles, releasing ACh?

A

Step 2

53
Q

Vesicular docking proteins are found where?

A

Synaptic vesicles

54
Q

What do vesicular docking proteins allow synaptic vesicles to do?

A

Attach at the presynaptic terminals rich in membrane docking proteins

55
Q

Depolarization triggers (influx, or efflux) of Ca

A

Influx

56
Q

Increase in Ca concentration induces what?

A

Exocytosis of synaptic vesicles and releasing ACh

57
Q

What step is AChE terminates the signal by hydrolyzing Ach into forming choline and acetyl CoA?

A

Step 3

58
Q

How can Ach be enzymatically degraded and where?

A

In the synaptic cleft by acetylcholinesterase (AChE)

59
Q

Where is AChE found?

A

Located in the post-synaptic membranes

60
Q

Hydrolyzing ACh forms what?

A

Choline and acetyl CoA

61
Q

Choline can be re-uptaked back to pre-synaptic terminal and recycled back into forming (-) by (-)?

A

ACh by Choline acetyltransferase

62
Q

Kinesin-mediated that carries cargos from axon terminal toward soma are (anterograde, retrograde)

A

Anterograde

63
Q

Dynein-mediated that carries cargos from axon terminal toward soma are (anterograde, retrograde)

A

Retrograde

64
Q

Axonal transport requires 3 things:

A
  • axonal cytoskeleton
  • motor proteins (kinesin and dynein)
  • hydrolysis of ATP
65
Q

What are the 2 motor proteins?

A

Kinesin and dynein

66
Q

Anterograde transport of vesicles and mitochondria is mediated by what?

A

Kinesin

67
Q

Retrograde transport of a vesicle along a microtubule is mediated by what?

A

Dynein

68
Q

Rabies virus is a neurotropic virus that is able to infect what?

A

Nerve cells

69
Q

Rabies virus is capable of binding to the (-) and replicates in the (-)

A

Acetylcholine receptor, muscle tissue

70
Q

The viral rabies particle migrated by (-) to the (-)

A

retrograde axonal transport to the cell body of neurons supplying affected muscle

71
Q

Does rabies virus continue to replicate within infected neurons? Where does this occur?

A

Yes, in the CNS

72
Q

Rabies virus is transported by (-) by the peripheral nerves to the (-)

A

Anterograde axonal transport, salivary glands

73
Q

How is rabies transported?

A

Transmitted by the bite

74
Q

A potent neurotoxin produced by clostridium tetani is what?

A

Tetanus

75
Q

Tetanus uses (-) to enter the (-)

A

Retrograde axonal transport to enter the CNS

76
Q

What does tetanus cause?

A

Spasm contraction of jaw, exaggerated reflexes, respiratory failure

77
Q

Tetanus blocks the release of (-) a the spinal synapse

A

Inhibitory mediators

78
Q

Varicella zoster causes

A

Chicken pox and shingles

79
Q

Zoster virus enter the nerve body using (retrograde, anterograde) axonal transport and stay (-) in the nerves

A

Retrograde, dormant

80
Q

Zoster virus reactivated by (-) and uses (anterograde, retrograde) axonal transport to move to nerve ending

A

Stress, anterograde

81
Q

Shingles starts at the muscle and then is transported to the skin (T/F)

A

True

82
Q

Curare produces what symptoms?

A

Muscle paralysis

83
Q

Curare bind to Ach receptor and prevents binding of Ach to the (-)

A

Nicotinic acetylcholine receptors

84
Q

Nicotinic acetylcholine receptors are located where?

A

Postsynaptic membrane

85
Q

Botulinum toxin is an exotoxin that prevents the release of (-) at the (-)

A

Acetylcholine at the presynaptic terminal

86
Q

Botulinum toxin produces what symptoms?

A

Muscle paralysis and dysfunction of the autonomous nervous system

87
Q

Myasthenia gravis is an autoimmune disease with antibodies against (-) which

A

Ach receptors which prevent binding of Ach to the nicotinic acetylcholine receptors

88
Q

Myasthenia gravis symptoms

A

Muscle weakness

89
Q

Lambert-Eaton myasthenic syndrome is an autoimmune disease with antibodies against (-)

A

Voltage-gated Ca channels

90
Q

Lambert-Eaton myasthenic syndrome reduces (-) into intracellular space

A

Calcium

91
Q

Lambert-Eaton myasthenic syndrome symptoms

A

Muscle weakness

CPPS 302 (14 decks)

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