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HOM > Muscle > Flashcards

Muscle Flashcards

1
Q

Which of actin/myosin is thick and which is thin?

A

Actin = thin, myosin = thick

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2
Q

Which troponin subunit binds to Ca2+?

A

C subunit

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3
Q

What is the physical chain of events of the cross bridge cycle?

A

Detatch, attatch, rotate, unit force

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4
Q

What are the two states of myosin?

A

Ground or activated

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5
Q

What is maximum force called in a muscle?

A

Isometric

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6
Q

Which muscle type doesn’t have troponin?

A

Smooth

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7
Q

How is contraction initiated in smooth muscle?

A

Ca2+-regulated phosphorylation of myosin by MLCK

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8
Q

What does Ca2+ bind to in order to activate MLCK?

A

Calodulin

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9
Q

How do you form a latch bridge in smooth muscle?

A

Remove phosphate when the cross bridge is formed

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10
Q

How many Ca2+-binding subunits does troponin subunit C have? How many are high-affinity regulatory?

A

4,2

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11
Q

What causes the upstroke and downstroke of the early surface wave?

A

Upstroke = Na+ channel activation, downstroke = Na+ channel deactivation, K+ channel activation, Cl- channel stabilises

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12
Q

Where must muscle be stimulated to get a contraction? Why?

A

Z lines because this is where tubular system is

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13
Q

What do DHP channels do?

A

Modified Ca2+ channels which detect voltage change and change configuration so interact and open Ryanodine receptor

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14
Q

What do “junctional folds” do?

A

Have active zones which contain the transmitter

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15
Q

What is in the synaptic cleft?

A

Nucopolysaccharide “glue” and has extracellular material called the “basal lamina”

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16
Q

Which enzymes makes ACh?

A

Choline acetyltransferase

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17
Q

Where is ACh localised to?

A

Basal lamina

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18
Q

What does “I” and “A” band stand for?

A

Isotropic, anisotropic

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19
Q

What is the selectivity filter of the ACh receptor?

A

Hydrophilic amino acids pointing inwards, rejects anions but cations can pass through

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20
Q

What makes up myosin?

A

Two twisted meromyosin strands (heavy head with S1 and S2 part and light tail)

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21
Q

What activates ATPase which reacts with actin?

A

MLCK

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22
Q

What does the cardiac muscle syncytium mean for its Ca2+ store?

A

More limited Ca2+ store

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23
Q

What is the process of the cross link cycle?

A

My and act both positively charged, need -ve phosphate to allow them to bind, phosphate is then lost so two +ve charges cause conformational change, another ATP needed so phosphate binds again and act and my let go

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24
Q

Why does heart have an intrinsic pacemaker rate?

A

Prolonged plateau and longer time to reach upstroke

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25
Q

What does effect of Cl- depend on?

A

Vm

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26
Q

Why is there a plateau in act pot?

A

Rapid upstroke from Na+ channels opening, these inactivate but Ca2+ channels open so depolarization maintained at 0mV until repolarisation by K+ channel

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27
Q

Stages of plateaued act pot?

A

Early rapid depolarisation, initial rapid depolarisation, plateau, terminal repolarisation, electrical diastole

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28
Q

Why does cardiac muscle show prolonged refractory period and have “excitability gap”?

A

To prevent tetanus, only one act pot for every beat

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29
Q

What is the T wave?

A

Ventricular repolarisation

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30
Q

What does the Na+-Ca2+ exchange in cardiac muscle cause?

A

Depolarisation

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31
Q

What is Ca2+ released by?

A

Phosphoinositide lipid

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32
Q

What is conduction like in the atria?

A

Poorly developed T system, wave of induced Ca2+ release, caveolae (membrane invaginations)

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33
Q

What does the funny current do?

A

The pacemaker current

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34
Q

What happens in the vagus nerve to the heart/what neurotransmitters are there?

A

Ach released in SA node, ACh and muscarinic K+ channel causes hyperpolarisation, needs longer funny current so HR down

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35
Q

What happens in the accelerator nerve to the heart/what neurotransmitters are there?

A

Sympathetic to all over the heart, NA and A from adrenal medulla increase rate of pacemaker depolarisation, enhanced Ca2+ channel activation, increased cAMP, more Ca2+ so higher heart rate, act pot shortened

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36
Q

Where is the AV node?

A

On the right where blood comes in

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37
Q

What causes the funny currents?

A

HCN channels in membrane open below threshold potential

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38
Q

What happens to DHP/RyR in cardiac muscle?

A

Aren’t linked, DHP is now a calcium channel which changes conformation, Ca2+ enters cell and binds to RyR allowing more Ca2+ release (Ca2+-induced Ca2+ release) so more contraction

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39
Q

How does cAMP affect HCN?

A

Increases leak to increase heart rate

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40
Q

How does ACh affect cAMP?

A

Decreases cAMP so decreases HCN leak so heart rate slows

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41
Q

Why does Ca2+ contribute to the action potential in cardiac muscle?

A

Because it crosses the membrane

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42
Q

Why does myotonia congenita occur?

A

Cl- channels have defect causing sustained muscle tension

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43
Q

Why isn’t much K+ required for a high concentration in the T tubules? Which channels make sure the cell still goes negative?

A

The T tubules are small, Cl-

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44
Q

What is a MEPP?

A

Miniature end plate potential, random release of vesicles from Ca2+ leaking

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45
Q

What are the subunits in nicAChR?

A

5 subunit, 2 where ACh binds (alpha) then beta gamma and delta.

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46
Q

What is a motor unit?

A

All muscle fibres innervated by one nerve

47
Q

What influences the frequency of MEPPs?

A

[Ca2+], [Mg2+], [K+], osmotic pressure

48
Q

What are the steps to test the NaKATPase?

A

Inject radio-labelled ATP, will drop as there’s less in cell so harder to pump out, remove all K+ ions so drops but can still use Na+ to stay working, check it’s not broken, add DNP and it slows, wash away and check again

49
Q

How do you test the electrogenic effect of the NaKATPase?

A

Rubbing skin causes lot of act pots and membrane potential drops (pup overactive and Na+ in continuously), if you hyperpolarise it too much you can’t reach the threshold pot

50
Q

How do you get malignant hyperthermia?

A

Anaesthetic gas and RyR

51
Q

Which muscle’s method of contration doesn’t affect the act pot?

A

Skeletal

52
Q

When are inwardly rectifying channels open?

A

When cell is negative

53
Q

Which stroke is which is pacemaker potentials?

A

Na Ca K

54
Q

How do hormones affect calmodulin?

A

Hormone to PLC to PLC to calmodulin

55
Q

Which enzyme forms the latch bridge?

A

Myosin phosphatase

56
Q

Where do you find MSP

A

At end of capillaries

57
Q

What is the ANREP effect?

A

Heart contracts harder and ejects more so end systolic volume is reduced instead of being the same each time

58
Q

Which receptors in parasympathetic?

A

NicAChR then muscAChR

59
Q

Which receptors in sympathetic?

A

nicAChR then NA

60
Q

Why do you get larger force for same Ca2+ release with NA?

A

Only two Ca2+ needed

61
Q

Which muscle type has no sarcomeres?

A

Smooth

62
Q

What is the anchor in smooth muscle?

A

alpha-actinin

63
Q

What is the control of the crossbridge cycle called in smooth muscle?

A

Covalent regulation

64
Q

What phosphorylates caldesmon? What activates this?

A

PKC activated by DAG

65
Q

What is a second messenger which open Ca2+ channel in the SR in smooth muscle

A

IP3 from PIP2 (made when receptors activate PLC)

66
Q

What is the secondary activate transport in cardiac muscle?

A

Sodium calcium exchange (one Ca out, three Na in)

67
Q

Which muscle type has dyad rather than triad junctions?

A

Cardiac

68
Q

What does inward rectification do?

A

Increases membrane resisitance and reduces calcium flow that’s generating the plateau so minimises Ca2+ gradient dissipation, minimises leak currents and therefore reduces the amount of inward current reuqired to sustain the plateau phase of the cardiac muscle action potential

69
Q

How many binding sites does troponin have in cardiac muscle?

A

Three not four

70
Q

How is contraction strength regulated in cardiac muscle?

A

Amount of Ca2+ because one excitation stimulates all muscle cells

71
Q

What stabilises the AChR pentamer?

A

Lipophilic side chains point outwards towards the hydrophobic interior of the lipid bilayer

72
Q

Why is the EPSP slower than the EPSC?

A

Because of the time necessary to charge and discharge the muscle membrane capacitance

73
Q

What happens to the EPSC as Vm gets larger and larger?

A

First gets smaller, then disappears, then gets larger in the opposite outward direction

74
Q

What is the reversal potential of the EPSC?

A

0 mV

75
Q

Why do EPSCs speed up with depolarisation?

A

Some voltage-dependence of the ACh gating (energy efficient because the conductance switches off faster when it’s no longer needed for depolarisation)

76
Q

What is the active ingredient of curare?

A

D-tubocurarine

77
Q

How does curare work?

A

Competes with ACh for binding on post-synaptic receptor but can’t cause channel opening

78
Q

What does eserine/physostigmine do?

A

Blocks acetylcholinesterase in the synaptic cleft so can measure how much ACh is released

79
Q

What does alpha-bungarotoxin do?

A

Binds tightly to and blocks AChR so if you radioactively label it you can count the AChRs

80
Q

What does alpha-latrotoxin do?

A

Massive release of pre-synaptic transmitter causing neuromuscular block by ACh depletion

81
Q

What does botulinum toxin do?

A

Prevents ACh release

82
Q

What changes MEPP frequency?

A

Decreased by decreased internal calcium or increasing magnesium, increasing by increasing external K+ or osmotic pressure

83
Q

What is a consequence of the cable properties of muscle?

A

Without regenerative, inward current through voltage gated Na channels, the depolarisation fades with distance and more and more of the endplate current leaks away

84
Q

Abnormalities in which protein have been associated with the pathogenesis of muscle dystrophy?

A

Dystrophin

85
Q

What are the light and heavy strands of myosin made from?

A

Meromyosin

86
Q

Where is the ATPase activity in the myosin head?

A

The S1 fraction

87
Q

What is the structure of tropomyosin?

A

Rod shaped, forms alpha helical subunits which get packed into the groove formed by intertwisted helical actin chains

88
Q

What are the three troponin subunits?

A

TnC, TnT and TnI

89
Q

Where does tropomyosin go during activation?

A

Deeper into the actin groove

90
Q

Which part of myosin is flexible?

A

Link between S1 and S2 segments

91
Q

How many twitches is there enough ATP for in the cell?

A

8

92
Q

How many twitches is there enough phosphocreatine for?

A

100

93
Q

How many of the TnC binding sites have high Ca2+ affinity?

A

Two out of four

94
Q

How much of the total tubular surface area do triads make up?

A

70%

95
Q

Why do resting skeletal muscle cells show chloride conductance?

A

Stabilises membrane potential between electrical activity episodes

96
Q

Why do you get myotonia congenita?

A

Deficiency/absence of functioning chloride channels causing repetetive action potential firing

97
Q

What results from conformational changes of voltage sensor?

A

Small currents or charge movements

98
Q

In skeletal muscle what does the elevated cytosolic calcium represent?

A

Release from SR stores (none from extracellular space)

99
Q

What triggers malignant hyperthermia?

A

Halothane (RyR defect)

100
Q

What moves calcium back to the SR?

A

Ca-ATPase (two calcium per one ATP)

101
Q

What is calsequestrin binding ratio for calcium?

A

1:45

102
Q

What are the five phases of the ventricular action potential?

A

Very rapid depolarisation, initial brief rapid repolarisation, plateau, terminal repolarisation, electrical diastole

103
Q

How often do the SA node pacemaker cell discharge?

A

60-80 times/min

104
Q

How often do the AV node cells discharge?

A

40-60 times/min

105
Q

How often do the Purkinje cells discharge?

A

30-40 times/min

106
Q

What takes over if there is severe SA node inhibition?

A

AV node or Purkinje fibres

107
Q

WHat is different in conducting tissues of the heart?

A

Fewer myofilaments, faster impulse generation and propogation, can function as pacemakers

108
Q

WHy does SA node determine overall HR?

A

Highest automaticity

109
Q

WHat are the two His bundle fans called?

A

Right (smaller) and left

110
Q

What is the left His bundle divided into?

A

Anterior and posterior

111
Q

Why is smooth muscle spiking activity not prevented by tetrodotoxin?

A

Produced by voltage gates Ca2+ channels

112
Q

What restores cytosolic calcium levels in cardiac muscles?

A

Ca-ATPase pumps, Na-Ca exchange (uses Na gradient energy)

113
Q

How does digitalis and other cardiac glycosides work?

A

Block sodium pump and allow increase in intracellular sodium concentration

114
Q

What is the Bowditch effect?

A

Myocardial contractility increases with heart rate

HOM (7 decks)

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