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BMPH 1 > Muscle > Flashcards

Muscle Flashcards

1
Q

What triggers muscle contraction?

A

Action potentials initiated in spinal cord motor neurons and conducted to muscles via motor axons

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2
Q

How many neurons innervate a skeletal muscle fiber?

A

1

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3
Q

How many muscle fibers can a motor neuron innervate?

A

Multiple

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4
Q

Neuromuscular junction (NMJ)

A

connection between the motor nerve terminal and muscle

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5
Q

Connection between the motor nerve terminal and muscle

A

neuromuscular junction (NMJ)

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6
Q

What type of synapse is the NMJ?

A

chemical

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7
Q

Motor nerve terminal

A

Presynaptic element of NMJ

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8
Q

Muscle endplate

A

postsynaptic elect of NMJ

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9
Q

presynaptic element of NMJ

A

motor nerve terminal

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10
Q

postsynaptic element of NMJ

A

muscle endplate

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11
Q

How does skeletal muscle excitation work?

A

1) AP reach motor nerve terminal
2) depolarization open Ca2+ channels
3) Ca2+ move down gradient into motor nerve terminal, inc cytosolic [Ca2+]
4) Ca2+ binds to multiple intra-terminal proteins (synaptotagmin) intitiating exocytotic release of vesicles docked nearby
5) Ach in vesicles diffuses across cleft and binds to nicotinic Ach receptors in muscle endplate
6) Non-specific cation channels (K, Na, Ca) open, allowing Na and Ca in
7) Results in depolarization, which initiates AP in muscle
8) AP travels into interior of muscle via transverse tubules (t-tubules)

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12
Q

What happens when the action potential reaches the motor nerve terminal?

A

Depolarization opens Ca channels

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13
Q

What role does Ca play in muscle excitation presynaptically?

A

Opening of Ca channels causes influx of Ca into local cytosol, which binds to intra-terminal proteins and initiates exocytotic release of NT Ach in nearby vesicles

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14
Q

Where does Ach bind on motor endplate?

A

nicotinic Ach receptors

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15
Q

What happens when Ach binds to receptors on motor end plate?

A

Opens non-specific cation channels, allowing Na and Ca

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16
Q

What is the result of the influx of Na and Ca postsynaptically in muscle excitation?

A

Depolarization, which starts an AP in muscle

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17
Q

How does the AP travel in the muscle?

A

via T-tubules

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18
Q

How long does muscle excitation take?

A

0.5 ms

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19
Q

What happens to Ach after muscle excitation?

A

Hydrolysed to acetate and choline by acetylcholinesterase in cleft. Choline is transported back to motor nerve terminal to resynthesizes into Ach.

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20
Q

Obligatory synapse

A

An AP in presynaptic motor nerve terminal always releases enough ACh to produce a depolarization that exceeds threshold for starting an AP in the muscle

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21
Q

What are the structure of skeletal muscle from larger to small?

A

Muscle > muscle fibers > myofibril > sarcomere

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22
Q

What is the structure of the sarcomere?

A 
z-line 
~=myosin (surrounded by 2 actin)
-=actin
no actin=H band
myosin=A band
actin only=I band

~~~~~~~~~~~~~~~~~~~~~~~ |
|—————- ——————-|
| ~~~~~~~~~~~~~~~~~~~~~~~ |

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23
Q

How do skeletal muscle contract?

A

1) AP in T-tubules leads to activation of ryanodine receptors in sarcoplasmic reticulum (SR)
2) Ca2+ released from SR into cytosol throughout the muscle
3) elevated cytosolic Ca2+ can trigger additional release of Ca2+ from SR (Ca2+ induced Ca2+ release, CICR)
4) elevated cytosolic Ca2+ activates contraction cycle

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24
Q

Sarcoplasmic reticulum (SR)

A

Specialized endoplasmic reticulum that stores Ca2+

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25
Q

Ca-induced Ca release (CICR)

A

Elevated cytosolic Ca triggers additional release of Ca2+ from SR

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26
Q

How does the Actin-myosin contractile cycle work?

A

1) Cytosolic Ca finds to troponin
2) confirmational change that rotates tropomyosin out of the way so actin can bind to myosin heads
3) Binding forms cross bridges that release energy stored in myosin head (ADP+P so P release)
4) Myosin head moves along the actin filament (power stroke)
5) crossbridge is broken when ATP binds to myosin head again

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27
Q

How does the sarcomere change with muscle contraction?

A

Sarcomere shortens but lengths of actin and myosin do not

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28
Q

What happens when ATP is not present?

A

Muscle contraction does not stop, so muscle become rigid (ex: rigor mortis)

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29
Q

How does the SR take up Ca2+?

A

via sarcoplasmic endoplasmic reticular Ca2=-ATPase (SERCA) pumps

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30
Q

How are SERCA pumps regulated?

A

By phospholambins

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31
Q

What are the types of contractions?

A

Isotonic, isometric, twitch, and tetanus

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32
Q

What is an isotonic contractions?

A

Muscle shortens (ex: pick up a light object like a phone)

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33
Q

What is an isometric contraction?

A

Muscle does not move (ex: lift something very health like a desk)

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34
Q

What is a twitch?

A

The contraction that follows a single muscle action potential

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35
Q

What is the active component of a twitch?

A

Depends on cross bridge cycle

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36
Q

What is the passive component of a twitch?

A

Depends on elastic elements in muscle, tendons, and structures the tendons are attached to, which all contribute to the way muscle force develops and exerts force on bones. They distribute force in time.

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37
Q

What is a tetanic contraction?

A

contraction produce by rapid repetitive stimulation

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38
Q

How is tetanus possible?

A

Muscle AP is much shorter than contraction, so muscle can be stimulated multiple times before CA from first AP has been sequestered. Thus, Ca accumulates in the cytosol.

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39
Q

What is the role of dystrophin?

A

Helps attach the plasma membrane to cytoskeleton, which prevents muscles from being mechanically fragile and prevent progressive muscle destruction like muscular dystrophy.

40
Q

What is a motor unit?

A

A motor neuron and all the skeletal muscle fibers it innervates

41
Q

What is myoglobin?

A

A protein that helps supply oxygen throughout the cell (higher affinity to oxygen than hemoglobin)

42
Q

What are the different types of skeletal fibers?

A
  • Slow (1, slow)
  • fatigue resistant (2A, fast oxidative)
  • fast fatiguing (2B, glycolytic)
43
Q

What are the characteristics of slow fibers?

A 
Myosin ATPase turnover: low
Diameter of individual cells: small
Myoglobin Concentration: high
Color: red
# of mitochondria: many
Fatigue: resistant
Glycogen stores: moderate
44
Q

What are the characteristics of fatigue resistant fibers?

A 
Myosin ATPase turnover: high
Diameter of individual cells: small/intermediate
Myoglobin Concentration: high
Color: red
# of mitochondria: many
Fatigue: resistant
Glycogen stores: high
45
Q

What are the characteristics of fast fatiguing fibers?

A 
Myosin ATPase turnover: high
Diameter of individual cells: large
Myoglobin Concentration: low
Color: white
# of mitochondria: fewer
Fatigue: fatiguable
Glycogen stores: very high
46
Q

How do the muscle fiber types differ?

A
  • Slow has low myosin ATPase turnover
  • diameter: slow>FR>FF
  • fast fatiguing have low myoglobin, are white, have fewer mitochondria, and are fatiguable
  • Glycogen stores: FF>FR>slow
47
Q

How are the muscle fiber types similar?

A
  • FR & FF: high myosin ATPase turnover

- Slow & FR: high myoglobin concentration, red, many mitochondria, and fatigue resistant

48
Q

How are cardiac muscle similar to skeletal muscles?

A
  • sarcomeres

- Ca2+ stimulates contraction using tropomyosin and troponin complex on actin filaments

49
Q

How are cardiac and skeletal muscles different?

A

Cardiac:

  • own pacemaker so no need for external innervation
  • Obtain Ca2+ from SR and from across membrane
  • longer AP similar to contraction duration (no tetanus possible)
  • Activity with neighboring cells synchronized by gap junctions
50
Q

How are smooth muscles similar to cardiac and skeletal?

A
  • Ca2+ dependent contractions mediated by actin and myosin
51
Q

How do smooth muscles differ from cardiac and skeletal?

A
  • Not arranged in sarcomeres

- contraction mechanism: calmodulin, IP3 instead of ryanodine receptors

52
Q

What is the contraction mechanism in smooth muscles?

A

1) Ca binds to calmodulin
2) Ca-calmodulin complex activates myosin light chain kinase (MLCK)
3) MLCK phosphorylates the light chain of myosin
4) conformational change in myosin to give rise to activated states
5) Actin-myosin cross bridge cycling like in skeletal
6) Contraction ends when phosphatase removes activating phosphate

53
Q

How do the muscle types differ in terms of nucleation?

A

Skeletal: multi
Cardiac: 1-2
Smooth: 1

54
Q

How are the muscle types organized?

A

Skeletal and cardiac: sarcomeres

Smooth: no sarcomeres

55
Q

How do the muscle types source Ca2+?

A

Skeletal: intracellular
Cardiac: extra and intracellular
Smooth: extra and/or intracellular

56
Q

How do the muscle types use Ca2+ for contraction?

A

Skeletal and cardiac: Ca acts on troponin on thin filament

Smooth: Ca acts on calmodulin, regulating thick filament

57
Q

What types of contracts can the muscle types do?

A

Skeletal: twitch and tetanic
Cardiac: no tetanic
Smooth: variable twitch duration and variation tetanic contraction

58
Q

What is the length of APs compared to contraction for muscle types?

A

Skeletal: AP < contraction
Cardiac: AP = contraction
Smooth: variable

59
Q

What ions are involved in the APs of each muscle type?

A

Skeletal: Na
Cardiac: Na and Ca
Smooth: Na and/or Ca

60
Q

How does contraction work for each muscle type?

A

Skeletal: triggered by 1 motor neuron
Cardiac: triggered by pacemaker while neurons modulate pacemaker rate
Smooth: NTs, hormones, local factors, etc.

61
Q

What is myasthenia gravis and how is it treated?

A

Antibodies again EACh receptors reduce endplate potential amplitude.

Use drugs to inhibit ACh breakdown by ACh-esterase

62
Q

What is Lamber-Eaton myasthenic syndrome and how is it treated?

A

Antibodies bind to motor nerve terminal Ca channels, reducing Ca entry and thus EACh release

K channel blocker to inc duration of presynaptic AP, allowing more Ca antra. Also use drug to inhibit EACh breakdown

63
Q

What is malignant hyperthermia and how is it treated?

A

Complication associated with inhaled anesthetics: high fever and muscle rigidity associated with mutant ryanodine receptors, causing excessive channel opening.

Block RyR (dantrolene). Standard muscle relaxants don’t work.

64
Q

What is Duchenne muscular dystrophy and how is it treated?

A

Mutations in dystrophin that links to complex that links cytoskeleton with extracellular matrix (important for mechanical stability of sarcolemma).

65
Q

What are the 3 main mechanisms for transporting molecules across the plasma membrane?

A

1) ion channels: passive transport
2) transporters: both passive and secondary active transport
3) pumps: primary active transport

66
Q

What is active transport?

A

Goes against the gradient and therefore requires and energy source.

67
Q

What are the two types of ion channels?

A

1) non-gated: always open

2) gated: open only at certain times

68
Q

What are the 3 types of gated ion channels?

A

1) mechano-sensitive
2) voltage-sensitive
3) chemo-sensitive

69
Q

Describe the Na/K-ATPase pump.

A

1) Primary-active ion pump.
2) Couples transport of the ions to the hydrolysis of ATP.
3) Generates non-equilibrium distribution of Na and K in intra/extracellular spaces.

70
Q

What are secondary-active transporters?

A

Utilize free energy stored in concentration gradient of Na across the membrane to drive uphill transport of an ion or solute

71
Q

Why is movement through an open channels so much greater than primary or secondary active transporter?

A

Transporters need to change shape each time

72
Q

How can we determine whether transmembrane transport of a solute is active or passive?

A
  • Solute is uncharged: Concentration gradient only

- Solute is charged: concentration gradient and electrical gradient

73
Q

What happens when Na channels open?

A

Concentration and voltage gradients favor Na entry

74
Q

What happens when K channels are open?

A

Concentration gradient: exit

Voltage gradient: entry

75
Q

What happens when Cl channels are open?

A

Concentration gradient: entry

Voltage gradient: exit

76
Q

What is the resting membrane potential?

A

The transmembrane voltage is close to the equilibrium potential of K because at the RMP the # of K channels open far exceeds the # of open NA of Ca channels.

77
Q

On what ion does the resting membrane potential depend on?

A

Extracellular K concentration

78
Q

What happens if extracellular [K+] is reduced?

A

RMP more negative: hyperpolarization

79
Q

What happens if extracellular [K+] is increased?

A

RMP less negative: depolarization

80
Q

What is an action potential?

A

A transient, populated depolarization produced by a sequence of ion channel openings and closings.

81
Q

What is the mechanism of an action potential?

A

1) depolarization activated NA channels open
2) Na influx drive membrane potential close to Na equilibrium
3) Na channels go into inactivated, closed stated
4) Depolarization activated K channels open (may differ from those open at RMP)

82
Q

What is a threshold?

A

The voltage level produced by a stimulus that evokes an action potential 50% of the time.

83
Q

What effect does changes in extracellular [Ca2+] concentration have on the threshold?

A

Hypercalcemia: raises threshold –> reduce excitability

Hypocalcemia: lowers threshold –> hyperexcitability

84
Q

What increases the speed of action potential propagation?

A

1) increase cell diameter

2) myelination of axons

85
Q

How are action potentials regenerated down the axons?

A

Nodes of ranvier in between myelin sheaths

86
Q

In glycolysis, which enzymes consume ATP?

A

Hexokinase (HK) and phosphofructokinase-1 (PFK-1)

87
Q

In glycolysis, which enzymes generate APT?

A

phosphoglycerate kinase (PGK) and pyruvate kinase (PK)

88
Q

In anaerobic glycolysis, which enzyme is required to re-oxidize NADH to NAD+, needed for glyceraldehyde 3-P dehydrogenase?

A

Lactate dehydrogenase

89
Q

In aerobic glycolysis, which enzyme is required to re-oxidize NADH to NAD+?

A

glycerophosphate dehydrogenase

90
Q

In the TCA cycle, which enzymes produce both NADH and CO2?

A

Isocitrate dehydrogenase and alpha-keoglutarate dehydrogenase

91
Q

In OxPhos, which pump protons from NADH-derived electrons?

A 
NADH dehydrogenase (Complex 1)
Cytochrome bc1 (Complex 3)
Cytochrome oxidase (Complex 4)
92
Q

In OxPhos, which pump proton form FADH2-derived electrons?

A 
Cytochrome bc1 (Complex 3)
Cytochrome oxidase (Complex 4)
93
Q

In OxPhos, which complex makes FADH2 but doesn’t oxidize is (pump protons from it)?

A

Succinate dehydrogenase (Complex 2)

94
Q

How is the release of Ca2+ from the skeletal muscle SR normally achieved?

A

Activation of dihydropyridine (DHP) receptors in transverse (T) tubules causes opening of ryanodine receptor (RyR) channels in SR membranes

95
Q

Which of the following best describes mechanisms that help synchronize smooth muscle contractions?

A

Bursts of APs initiated by pacemaker like mechanism in smooth muscle propagate via gap junctions between smooth muscle cells.

96
Q

Suppose that a cell has an RMP of -70 mV and that in this cell the electrochemical potential for Cl- is -75 mV. What will happen to the membrane potential and Cl- ions when Cl-channels open?

A

Hyperpolarize and influx

BMPH 1 (8 decks)

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