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CAPS 301 T1 > Muscle Facts > Flashcards

Muscle Facts Flashcards

1
Q

Arrangement of Sarcoplasmic Reticulum in skeletal muscle

A

Dense network of tubules outside of each myofibril, forming terminal cisternae on either side of T-tubules

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2
Q

Describe excitation-contraction coupling in striated muscle

A

Via CICR: Calcium-Induced Calcium Release

  • AP travels down T-tubule
  • Dihydropyridine receptors (sarcolemma) open
  • Ca++ influx
  • Ryanodin receptors (SR) open
  • Ca++ released from sequestrin right beside receptors
  • muscle contraction
  • NCX (Na+/Ca++ eXchanger) pumps Ca++ back through the sarcoplasm
  • SERCA pumps CA++ back into SR
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3
Q

Role of motor end plate

A

Start AP across myofiber to T-tubules

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4
Q

Describe myotendinous junction (skeletal muscles)

A

Arrows (projections) of myofibers insert into connective tissue

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5
Q

What does the dystroglycan-containing complex bind?

A

F-actin inside the cell, basal lamina outside (through the sarcolemma)

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6
Q

Organization of skeletal muscles: connective tissue

A

Epimysium -> Perimysium -> Endomysium (decreasing density)

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7
Q

Describe how increasing [Ca++] leads to muscle contraction (in presence of ATP) in skeletal muscle

A
  • Ca++ binds troponin
  • Moves tropomyosin away from myosin-binding sites on actin
  • Myosin (bound to ADP & Pi) binds actin (forming cross-bridge)
  • Power stroke drags actin towards M-line of sarcomere, releasing ADP & Pi
  • Myosin head binds ATP, releasing actin (removing cross-bridge)
  • ATP hydrolysis cocks myosin head
  • Repeat (from binding actin) until Ca++ removed & tropomyosin again covers myosin-binding sites
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8
Q

Role of dystroglycan-containing complex (skeletal muscles)

A

Allow cross-talk between the inside and outside of the myofiber (cell)

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9
Q

Motor neuron arrangement in skeletal muscle

A

Cell body in ventral horn of spinal cord; branches to have one axon terminal per myofiber in the motor unit

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10
Q

Two molecules needed for skeletal muscle contraction

A

Ca++, ATP

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11
Q

Arrangement of myofibrils in myofiber (skeletal muscle)

A

Parallel, separated by sarcoplasmic reticulum and mitochondria

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12
Q

Role of Sarcoplasmic Reticulum (all myocytes)

A

Store & release Ca++

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13
Q

Skeletal muscle function

A

Locomotion
Posture
Respiration (diaphragm & intercostal muscles)

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14
Q

Organization of skeletal muscles: muscle tissue

A

Muscle -> Fascicle -> Muscle fibers -> Myofibril (-> Myofilament *not “wrapped”)

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15
Q

Status of nucleus in skeletal muscles

A

Multi-nucleated; nuclei at periphery (just under membrane)

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16
Q

Location of sarcoplasmic reticulum & mitochondria in myofibers

A

Between myofibrils

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17
Q

Function of cardiac muscle

A

Heart beat

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18
Q

Symptoms of muscular dystrophy

A
  • Muscle wasting & degeneration
  • Mental retardation
  • Waddling tip-toe walk
  • Spinal curvature
  • Calf muscle pseudohypertrophy
  • Frequent falls, and inability to get up without use of arms
  • Poor fine motor skills
  • Weak diaphragm (trouble breathing -> lack ability to clear out pathogens -> may lead to death by pneumonia)
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19
Q

Effect of muscle stimulation with break in between

A

Muscle relaxes fully in between, resulting in two separate, same-size twitches

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20
Q

Cause of Becker Muscular Dystrophy

A

Mutation in dystrophin gene results in shortened (semi-functional) dystrophin protein

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21
Q

Result of two stimuli with partial muscle relaxation in between

A

Summation: second twitch is larger

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22
Q

Profile of dystrophin protein

A

N-terminus … actin-binding domain … rod-like domains w/4 hinge (Pro-rich) domains … Cys-rich domain (binds dystroglycan-containing complex) … C-terminus

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23
Q

Effect of botox

A

Botulism: prevents ACh release -> paralysis

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24
Q

Location of dystrophin gene

A

Short arm of X-chromosome; linked to muscular dystrophy

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25
Q

Result of prolonged, closely-spaced stimulation of muscle fibers

A

Tetanus: sustained maximal contraction because no relaxation between stimuli

26
Q

Cause of Duchenne Muscular Dystrophy

A

Mutation in dystrophin gene results in early stop codon -> shortened dystrophin protein missing Cys-rich domain is target for protein degradation (complete loss of function)

27
Q

Treatments for Muscular Dystrophy

A

Myoblast/stem cell transplant
Pharmacological treatment
Deliver DNA for microdystrophin (DMD only)
Exon skipping (DMD only)

28
Q

Describe exon skipping treatment for DMD & drawbacks

A

Use antisense oligonucleotide to cover the exon containing the early stop codon plus enough other codons to restore reading frame
Results in BMD (less severe than DMD)
Doesn’t work if stop codon is in a critical domain (e.g. Cys-rich or actin-binding domain)

29
Q

Result of Duchenne Muscular Dystrophy

A

Sarcomeres become unaligned, killing the myofiber

30
Q

Describe myoblast/stem cell transplant treatment for MD & drawbacks

A

Inject myoblasts or stem cells to replace lost myofibers

Difficult to inject large cells

31
Q

Result of muscular dystrophy

A

Holes produced in sarcolemma from force
Usually make new myocytes, but run out of ability
Holes filled with connective & adipose tissue

32
Q

Describe the pharmacological treatment for MD

A

Inject compound to increase utriphin expression (80% similar to dystrophin) to compensate

33
Q

Describe DNA delivery treatment for MD

A

Insert DNA for microdystrophin (short protein containing only components of dystrophin essential for semi-functional protein)

34
Q

Function of dystrophin/dystroglycan-containing complex

A

Force dissipation into basal lamina to prevent muscular degeneration over time

35
Q

Describe filament mechanism of contraction in smooth muscle

A
  • Contractile units (lateral) shorten
  • Pulls dense bodies and dense plaques closer together
  • Pulls “mesh” of thin filaments tighter around cell
36
Q

Compare response time of smooth and striated muscle, between signal and contraction

A

Slower in smooth muscle, typically

37
Q

Describe (autonomic) innervation and AP propagation in multi-unit smooth muscle

A
  • Abundant innervation by several autonomic innervation
  • Separated into independent contractile units
  • Few gap junctions
38
Q

Describe cardiac muscle fibers

A

Short, branched, attached at ends to other myofibers by intercalated disks; sarcomere arrangement similar to skeletal muscles

39
Q

Organization of smooth muscle around arteries and veins

A

Forms tunica media (middle layer); thicker in arteries to sustain higher pressures

40
Q

Location of multi-unit smooth muscle

A
  • hair follicles
  • large blood vessels
  • small airways in lungs
  • iris & lens of eye
41
Q

Form of intercalated disks

A

step-like: transverse and lateral components

42
Q

Organization of smooth muscle around intestines

A

Longitudinal & circular layers (coordinate for peristalsis; allow forwards movement only)

43
Q

Function of smooth muscle

A

Constriction of viscera and blood vessels

44
Q

Location of mitochondria and neurotransmitter vesicles in motor neurons for skeletal muscle

A

Axon terminal buttons

45
Q

What does smooth muscle have instead of T-tubules?

A

Caveolae (goblet-shaped)

46
Q

Describe (autonomic) innervation and AP propagation in single-unit smooth muscle

A
  • Less abundantly innervated by autonomic neurons than multi-unit
  • Many gap junctions - spread AP throughout
  • Single contractile unit (many myocytes contract together)
47
Q

Describe nuclear state of smooth muscle cells

A

1 central nucleus per myofiber, takes on corkscrew shape during contraction

48
Q

Organization of smooth muscle around stomach

A

Longitudinal, circular and oblique layers (allow food to be mixed in multiple directions)

49
Q

Describe pharmacomechanical coupling in smooth muscle fibers

A
  • NO CHANGE IN V_m*
  • Hormone/neurotransmitter binds membrane receptor
  • Increase cytoplasmic [IP3] (inositol triphosphate)
  • Bind IP3 receptors on peripheral SR face
  • Opens ligand-gated Ca++ channels
  • Usual mode of contraction via myosin & actin
50
Q

Component(s) of transverse region of intercalated disks (cardiomyocytes)

A
  • zonula adherens (attaches f-actin of terminal sarcomeres to plasma membrane)
  • desmosomes (keep adjacent fibers together during contraction)
51
Q

Organization of caveolae in smooth muscle fibers

A

Rows, alternating with rows of dense plaques

52
Q

Fact: Smooth muscle cells have no T-tubules

A

(fact)

53
Q

Component(s) of lateral region of intercalated disks (cardiomyocytes)

A

Gap junctions (allow free ion movement between cells for faster AP transmission)

54
Q

Describe general autonomic innervation of smooth muscle

A
  • Post-ganglionic nerve branches in muscle
  • Varicosities slightly removed from muscle
  • NT diffuses through the space
55
Q

Describe excitation-contraction coupling in smooth muscle

A
  • V-gated channels open: extracellular Ca++ into sarcoplasm
  • Ryanodin receptor releases Ca++ from SR (CICR)
  • Ca++ binds CALMODULIN
  • Ca++/Calmodulin binds MLCK
  • phosphorylates 2 myosin light chains
  • allows usual myosin contraction
56
Q

Location of mitochondria and neurotransmitter vesicles in motor neurons for smooth muscle

A

Varicosities

57
Q

Function of gap junctions in intercalated disks

A

Allow free ion movement between myofibers for faster AP transmission

58
Q

Location of single-unit smooth muscle

A
  • walls of viscera

- small blood vessels

59
Q

Describe filament arrangement in smooth muscle

A
  • Thin filaments arranged obliquely
  • “Mesh” anchors sarcomere in cell
  • Contractile units arranged laterally
  • Filaments attached to dense bodies (cytoplasm) or dense plaques (plasma membrane)
60
Q

Difference(s) between SR in cardiac and skeletal muscle

A

More sparse & contains less Ca++ in cardiac muscle; 1 cisterna per T-tubule

61
Q

Location of SR in smooth muscle fibers

A

Below caveolae (for sensitivity to Ca++ influx through dihydropyridine receptors)

CAPS 301 T1 (10 decks)

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