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Block 4: Cell Structure & Function > Muscle I and II > Flashcards

Muscle I and II Flashcards

1
Q

What is the name of the conventional myosin in muscle? What is its specific structure? What do its pieces contain?

A

Muscle myosin II. It is a hexamer with 2 heavy chains and 2 pairs of light chains. The heavy chain portion contains actin and the ATP binding site. (can only bind strongly to one or the other, but not both)

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2
Q

How many different types of myosin are there?

A

10 types

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3
Q

What is titin made out of? size? Is it motor, regulatory, or structural? What is its purpose during myogenesis? What type of tension is it responsible for?

A

Very large elastic protein. Structural. Serves as a molecular ruler during myogenesis. Responsible for passive length tension.

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4
Q

Is nebulin motor, regulatory, or structural? what type of muscle is it found in? What type of protein is it? How many per actin?

A

Structural. Found in skeletal muscle only. Long inelastic protein. 2 per actin.

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5
Q

What are the 4 regulatory proteins in muscle? What do they do?

A

All part of the troponin complex, except the last one.
Troponin-T: binds to tropomyosin and helps position it on the actin, which exposes the myosin-binding sites.
Troponin-I: binds to actin and prevents myosin from binding to it
Troponin-C: calcium binds to it causing a conformational change that disrupts the actin-TnI interaction
Caldesmon/Calponin: Smooth muscle only. acts similar to TnT and TnI

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6
Q

Explain the length-tension relationship: what if the fiber is too long/short?

A

Too long: Not enough cross bridge can form leading to less tension and force.
Too short: Thick filament clashes w/z disc leading to less tension and force.
optimal length of sarcomere: 2-2.25 micrometers

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7
Q
  1. is Type I muscle slow or fast twitch? How does it fatigue?
  2. Myoglobin color? metabolism type?
  3. Mitochondria and glycogen levels?
  4. size?
A
  1. Slow twitch, fatigue resistant
  2. Red myoglobin, oxidative metabolism
  3. High mitochondria, low glycogen
  4. small
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8
Q
  1. is Type IIa muscle slow or fast twitch? How does it fatigue?
  2. Myoglobin color? metabolism type?
  3. Mitochondria and glycogen levels?
  4. size?
A
  1. fast twitch, fatigue resistant
  2. red myoglobin, oxidative metabolism
  3. High mitochondria, abundant glycogen
  4. intermediate size
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9
Q
  1. is Type IIb/IIx muscle slow or fast twitch? How does it fatigue?
  2. Myoglobin color? metabolism type?
  3. Mitochondria and glycogen levels?
  4. size?
A
  1. fast twitch, fatiguable
  2. white myoglobin, glycolytic metabolism
  3. Fewer mitochondria, high glycogen
  4. Large in size
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10
Q

What does endurance training do to muscles?

A

Increase in type IIa fibers, mitochondria, and myoglobin. Decrease in type IIx fibers.

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11
Q

explain the L-type calcium channel, and what it causes to happen, all the way to troponin C

A

end plate potential turns into an action potential and then travels down t tubules where it activates the L-type calcium channels (DHP receptors). It then mechanically reacts with the ryanodine receptor RyR-1 to make Ca++ be released from the sarcoplasmic reticulum. The calcium binds to troponin C to increase Pi dissociation

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12
Q

In cardiac muscle instead of coupling with a ryanodine receptor, what happens?

A

calcium-induced calcium release with ryanodine receptor Ryr-2.

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13
Q

How does nore affect cardiac muscle?

A

it binds to beta andrenergenic receptors which increases Ca++ influx due to phosphorylation of Ca++ channels. Then you have calcium induced calcium release.

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14
Q

What does an overall increase in calcium due to heart contraxtion and relaxation

A

increased HR, contractility (inotrophy), and relaxation rate (lusitrophy). More rapid with more force.

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15
Q

Explain what calcium does in smooth muscle for thick filaments — Calcium DEPENDENT

A

For thick filaments:

  1. Calcium binds to calmodulin
  2. calcium calmodulin complex activates MLCK, which phosphorylates myosin light chain and allows it to interact with actin.
  3. The myosin light chain can stay in the phosphorylated state for a prolonged period of time forming myosin cross bridges (latch bridges) thus keeping smooth muscle tonically active.
  4. Myosin goes back to relaxed state once MLCP dephosphorylates the light chain. (MCCP can be activated by cGMP).
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16
Q

Explain what calcium does with thin filaments?

A

Calcium binds to caldesmon and calponin exposing tropomyosin and allowing MCL to bind to it. Caldesmon is similar to TnT and TnI in striated muscle.

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17
Q

What is Familial Hypertrophic Cardiomyopathy (HCM)

A

Leading cause of SCD. HCM is usually caused by a single amino acid mutation in the cardiac myosin heavy chain. The mutation changes ATP hydrolysis in the myosin which decreases force production leading to ventricular wall hypertrophy.

18
Q

What is malignant hyperthermia?

A

autosomal inherited myopathy due to defect in skeletal muscle ryanodine receptors Ryr-1. Characterized by uncontrolled muscle contracture and hyperthermia.

19
Q

What is cardiac hypertrophy and failure?

A

caused by reduction in cardiac muscle ryanodine receptors Ryr-2.

20
Q

What does Viagra do?

A

inhibits cellular breakdown of cGMP by blocking PDE5 and so enhances the effect of NO/cGMP, which causes the relaxation of smooth muscle. the localized relaxation of smooth muscle allows blood to swell in corpus cavernosum.

21
Q

What proteins help Ach vesicles fuse with membrane to enter the synaptic cleft?

A

SNARE proteins.

22
Q

The nicotinic-Ach receptor is what type of channel?

A

A ligand-gated sodium channel.

23
Q

In skeletal muscle, the L-type Ca++ channel (DHP) receptor let’s calcium flow in, in skeletal muscle.

A

False. Although called a calcium channel, in skeletal muscle calcium doesn’t actually flow through.

24
Q

What is myasthenia gravis? Involves what channel?

A

Blocking Ach receptors by AchR antibodies in the synapse.

25
Q

Difference between multi-unit and single unit smooth muscle?

A

multi-unit- each fiber can contract independently of others. Controlled independently by nerves.
single-unit- Aka visceral smooth muscle. Tight contact with gap-junctions.

26
Q

What is different about the DHP receptor in smooth muscle?

A

A TRUE voltage-gated Ca++ channel

27
Q

Instead of neuromuscular junctions, the ANS communicates with smooth muscle how? Via what?

A

autonomic nerves branch out onto the surface of smooth muscle and release neurotransmitters via varicocities.

28
Q

Smooth muscle: sympathetic NS uses what neurotransmitters and what receptor? Explain what happens depending on the receptor.
Cardiac muscle: B-adrengergenic receptor with nore does what?

A

epi/nore, onto alpha or beta adrenergenic receptors.
alpha— G alpha(q) uses IP3 DAG pathway to ACTIVATE SMOOTH MUSCLE CONTRACTION
Beta— G alpha(s) uses adenylate cyclase and cAMP pathway to INHIBIT CONTRACTION.
For cardiac Beta-receptor with nore, it increases HR (opposite of the smooth muscle)

29
Q

Smooth muscle: parasympathetic NS uses what neurotransmitter and what receptor? What is the overall effect?

A

G (alpha-q) protein. Uses Ach onto muscarinic receptors. uses Phospholipase C, IP3 DAG pathway to ACTIVATE SMOOTH MUSCLE CONTRACTION.

30
Q

Nitric oxide is what type of hormone?
Produced by what?
What pathway does it use, and what is the effect?
What drug helps it?

A

Paracrine hormone produced by endothelial cells.
Diffuses to nearby smooth muscle, using guanylate cyclase cGMP to inhibit Ca influx, resulting in RELAXATION OF SMOOTH MUSCLE. Viagra encourages this process.

31
Q

Explain calcium-independent contraction of smooth muscle.

A

Rho-Kinase cascade leads to phosphorylation of myosin light chain phosphatase, an enzyme that removes a phosphate from the myosin light chain. This deactivates this phosphatase, leaving it in an active phosphorylated state, which INCREASES contraction of smooth muscle.

32
Q

What do stretch receptors initiate? Important in what?

A

an intracellular cascade leading to calcium influx. Important in peristalsis.

33
Q

Explain spontaneous contraction of smooth muscle

A

In stomach, smooth muscle receives spontaneous “slow waves” from interstitial cells of Cajal (ICC) that result in action potentials when threshold is reached.

34
Q

More potassium leak channels open means what for smooth muscle?
What does 4-AP do?

A

More hyperpolarized the cell will be, and thus voltage-gated Ca++ channels will be closed.
4-AP is a potassium channel blocker. Results in membrane depolarization, and the opening of voltage gated calcium channels.

35
Q

What do catecholamines do in the heart?

A

activate intracellular cascades that lead to phosphorylation/activation of enzymes involved in heart rate, contractility, relaxation, and conduction speed (dromotropy).

36
Q

What effect does catecholamine have on phospholamban?

A

Phospholamban normally inhibits the SERCA pump, but is phosphorylated in response to catecholamine administration. Thus, SERCA activity increases, and cardiac muscle relaxes. However, this increases Ca++ concentration in the sarcoplasmic reticulum, so you get increased contractility upon stimulation.

37
Q

in endothelial cells, an increase in calcium does what?

In contrast, an increase in calcium in smooth muscle does what?

A

vasodilation, due to nitric oxide production.

in smooth muscle, it’s vasoconstriction.

38
Q

resting potential of smooth muscle?

A

-50 to -60 mv

39
Q

The delayed onset and prolonged contraction of smooth muscle is due to what?

A

Slower cycling rate of smooth m. myosin cross-bridge formation. However, it is strong (lots of bridges)

40
Q

An endplate potential occurs at the NMJ due to what fact? Think channels.

A

sodium permeability becomes much greater than potassium permeability. (NMJ channels are LIGAND gated, not voltage gated)

41
Q

What does BOTOX do?

A

Ach release blocker. Inhibition of vesicular fusion by inhibition of SNARE proteins.

42
Q

Calcium INDEPENDENT contraction of smooth muscle?

A

The intracellular signaling of the RhoA “Rho Kinase Cascade.”

  1. The activated RhoA kinase phosphorylates MLCP, which usually removes a phosphate from MLC. Instead, it gets its phosphate from RhoA so it is deactivated
  2. MLC is phosphorylated because it isn’t inhibited, so it can keep the smooth muscle contracted.

Block 4: Cell Structure & Function (3 decks)

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