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MD2002 > Excitation Contraction Coupling > Flashcards

Excitation Contraction Coupling Flashcards

1
Q

What does “excitation contraction coupling” refer to ?

A

Linkage between excitation of the muscle fibre membrane and the onset of contraction

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2
Q

What is the duration of skeletal muscle action potential ?

A

Around 10 ms

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3
Q

What events follow the generation of AP in skeletal muscle ?

A

Latent Period

Tension (contraction)

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4
Q

Which of the three kinds of muscles need(s) nerve stimulation ?

A

Skeletal Muscle

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5
Q

When does the latent period start, and end ?

A

At the peak of AP to the onset of change in tension

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6
Q

How may nerve stimulation affect the action of cardiac and smooth muscle ?

A

It may affect their rate of contraction

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7
Q

What is happening during the latent period (in skeletal muscle)?

A

“-Time taken for the stimulus to travel along the nerve to the neuromuscular junction

  • Time taken for the impulse to cross the neuromuscular junction and to stimulate the muscle
  • Time taken for the excitation-contraction coupling to occur”
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8
Q

What is the function of the sacroplasmic reticulum ?

A

Storing Ca2+

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9
Q

Which structure is responsible for the bringing the AP to muscle fibers during propagation at the motor end plate ? How does the morphology of skeletal muscle allow this to happen ?

A 
T tubule system, brings AP deep into the fiber.
Triad structure (T tubule sandwished between terminal cisternae) enables AP to propagate to muscle fiber and to talk to sarcoplasmic reticulum
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10
Q

How does depolarisation of the skeletal muscle fiber occur ?

A
  1. Somatic motor neuron release ACh at neuromuscular junction
  2. Net entry of Na+ through ACh receptor-channel activates voltage gated sodium and initiates a muscle action potential
  3. Action potential is propagated from the end plate along the surface of the muscle fibre (sarcolemma), then propagated into the fibre down the T-tubule membrane
  4. Depolarisation of the T-tubule membrane is ‘signalled’ to the membrane of the terminal cisternae
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11
Q

What is the stimulus causing a change in tension in skeletal and cardiac muscle ?

A

Intracellular Calcium

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12
Q

Where is calcium found in skeletal muscle ?

A

In the cytoplasm and in the sarcoplasmic reticulum/terminal cisternae

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13
Q

Is there a requirement for extracellular Ca2+ in skeletal muscle ?

A

NO

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14
Q

What is the mechanism of Calcium release in skeletal muscle ?

A
  1. Voltage gated Ca channels (DHPR) sense change in membrane potential in T tubule and undergo conformational change
  2. Activation allows interaction (mechanical coupling) with RYR (main channel responsible for release of Ca from stores)
  3. RYR then opens gate and allows Calcium to flow out into the cytoplasm
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15
Q

What is the trigger for release of calcium in skeletal muscle ?

A

Mechanical coupling between DHPR and RYR

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16
Q

What feature of the DHPR and RYR enables them to interact ?

A

Their close proximity to each other

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17
Q

What are the junctional foot proteins ? Which type of channel is each and where is each found ?

A

Dihydropyridine receptor protein (DHPR)- L-type voltage-gated calcium channel in the T- tubule membrane

Ryanodine receptor protein (RYR)- Calcium release channel in the SR (Ca2+ sensitive)

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18
Q

How does contraction occur, following calcium release, in both skeletal and cardiac muscle ?

A
  1. Release of Calcium activates troponin C

2. This enables strong actin-myosin binding

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19
Q

Why does Calcium flow out of the channel (given that it is not using energy) ?

A

The steep concentration gradient (lower concentration in the cytoplasm than in the SR)

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20
Q

How does the cytoplasmic concentration change from, before to after calcium release ?

A

Increases from < 10-7 M (100 nanoM) to > 10-5 M (10 microM)

21
Q

What is the excitation and what is the contraction in skeletal muscle ?

A

Excitation- Electrical signal (AP)

Contraction- Mechanical coupling driven by release of Ca+2 by sarcoplasmic reticulum

22
Q

What is the whole point of Calcium release ?

A

Getting cytoplasmic calcium concentration up to a point where it can interact with troponin C, leading to change in its conformation, allowing actin and myosin to interact, leading to contraction

23
Q

What is a drug which can target Dihydropyridines ? How does it work ? Which conditions is it used to treat ?

A

Nifedipine

Blocks voltage gated Ca2+ channels

Used to treat (smooth muscle)
– Hypertension
– Migraine
– Atherosclerosis

24
Q

What is a drug which can target Ryanodines ? How does it work ? Which conditions is it used to treat ?

A

Dantrolene

Used to treat
– Muscle spasm (because it is a skeletal muscle relaxant)
– Muscle rigidity in Malignant hyperthermia

25
Q

What is the underlying mechanism behind Malignant Hyperthermia ?

A

Point mutations in the gene coding for RyR1

26
Q

What are the symptoms of Malignant Hyperthermia ?

A
  • Muscle rigidity
  • High Fever
  • Increased acid levels in blood and other tissues
  • Rapid heart rate
27
Q

Which type of muscle does malignant hyperthermia affect ?

A

Skeletal Muscle

28
Q

Where do the first manifestations of MH usually occur ?

A

In the operating room, in reaction to commonly used anaesthetics and depolarising muscle relaxants

29
Q

Can malignant hyperthermia be fatal ?

A

If untreated, yes

30
Q

How does relaxation occur in skeletal muscle ?

A 
Increase in intracellular calcium concentration activates a Ca2+ ATPase (calcium pump) in the SR membrane
Calcium ATPase (SERCA) hydrolyses ATP 
For each ATP hydrolised, 2 ions of Calcium pumped from the cytoplasm into the SR
Cytoplasmic Calcium concentration are lowered (back to nanomolar levels) 
Troponin C gets back to origin shape, so no more interaction between actin and myosin
31
Q

What does SERCA stand for ?

A

Sarcoplasmic Endoplasmic Reticulum Calcium ATPase

32
Q

Which kind of transport does SERCA undertake (active, passive) ?

A

Active transport

33
Q

How does the cytoplasmic concentration change from, contraction to relaxation ?

A

Decrease from > 10-5 M (10 microM) to < 10-7 M (100 nanoM)

34
Q

Besides the fact that is being actively transported, what is another factor facilitating Calcium transport back into the SR given that the concentration gradient is not so steep ?

A

Calsequestrin, Calcium-binding protein within SR, can bind 43 calcium ions per molecule. Stores calcium at high concentrations in the terminal cisternae to establish a concentration gradient from the SR to the cytoplasm
Although lots of exchangeable Calcium, not a lot of free Calcium so when trying to get it back into the store, not working so much again concentration gradient because not very much free calcium in the sarcoplasmic reticulum

35
Q

What is the MW of calsequestrin ?

A

44 000

36
Q

How does innervation of cardiac muscle cells differ form innervation of skeletal muscle cells ?

A

Does not need to get innervated, because it has pacemaker cells.

37
Q

What are pacemaker cells ?

A

Specialised muscle cells
Unstable resting potential
Undergo automatic rhythmical depolarisation

38
Q

What is pacemaker potential ?

A

“Low depolarisation of the pacemaker cells e.g. cells of the sinoatrial node, towards threshold, allowing an action potential to be fired”

39
Q

How does autonomic innervation affect cardiac muscle ? Give examples of sympathetic and parasympathetic neurotransmitters, their innervation, and their effects on cardiac muscle cells action.

A

It may affect its rate.

Parasympathetic: Acetyl choline, slows rate and remains localised to pacemakers

Sympathetic: nor-adrenaline, increases rate and strength, and is diffuse

40
Q

Can heart muscle cells contract if they don’t receive signals from pacemakers cells ?

A

Yes, they all have intrinsic pacemaking ability

41
Q

How does depolarisation of the skeletal muscle fiber occur ?

A
  1. Pacemakers cells, undergo automatic rhythmical depolarisation
  2. Action potential is propagated from the end plate along the surface of the muscle fibre (sarcolemma), then propagated into the fibre down the T-tubule membrane
  3. Depolarisation of the T-tubule membrane is ‘signalled’ to the membrane of the terminal cisternae
42
Q

What is the mechanism of Calcium release in cardiac muscle ?

A
  1. Voltage gated Ca channels (DHPR) sense change in membrane potential in T tubule and undergo conformational change
  2. 25% of the Ca2+ required for contraction enters from the outside though DHPR in the transverse tubular membrane
  3. Calcium binds to RYR, opens it, and Ca2+ flows out (75% of Calcium required to trigger contraction) of the SR down its concentration gradient into the cytoplasm
43
Q

How much does the cytoplasmic concentration of Calcium have to increase to trigger contraction in cardiac muscle cells ?

A

From < 10-7 M to > 10-5 M

44
Q

What is the duration of a cardiac AP ?

A

Over 300 ms

45
Q

What is the main difference in the shape of the graph for cardiac muscle AP and skeletal muscle AP ?

A

Longer duration of cardiac AP

Plateau period in cardiac muscle

46
Q

What is the plateau period in the cardiac muscle AP due to ?

A

Depolarisation is fast, through fast activated voltage gated sodium channels.
Those channels deactivate quickly but then threshold reached and activate voltage gated calcium channels and calcium will flow through and cause extension of action potential (plateau region) thats where tension occurs (Calcium ions inflow causing release of Calcium).

47
Q

Why is there no latent period in cardiac muscle ?

A

Because as calcium flows in, it exends the AP so get the plateau period

48
Q

How does relaxation occur in cardiac muscle cells ?

A
  • Requires a decrease in cytoplasmic Ca2+ concentration from >10-5 M to < 10-7 M
  • Ca2+ ATPase in sarcoplasmic reticulum is activated, pumping out some Calcium into the SR. Calsequestrin helps, given that calcium is transported against its concentration gradient (so that no free calcium, allowing calcium to get into the stores).
  • Some Calcium also transported out of the cell through Na+:Ca2+ exchange in the sarcolemmal membrane (3 Na+ in :1 Ca+2 out)
  • To prevent Sodium generating an AP, pumps sodiums out and potassium in

MD2002 (77 decks)

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