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Physiology > skeletal muscle an the neuromuscular junction > Flashcards

skeletal muscle an the neuromuscular junction Flashcards

1
Q

characteristics of skeletal muscle

A
  • striated
  • voluntary: somatic innervation
  • multinucleated
  • contain satellite cells for repair
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2
Q

name skeletal muscle organization from muscle fibers to myofilaments

A
  • muscles are composed of muscle fibers
  • muscle fibers are composed of bundles of myofibrils
  • myofibrils consist of a bundle of parallel microfilaments called myofilaments
  • myofilaments are organized into contractile units called sarcomeres
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3
Q

what is the smallest functional unit of skeletal muscle

A

sarcomere

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4
Q

what are the two types of myofilaments

A
  • myosin
  • actin
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5
Q

How many neurons innervate one fiber at one location?

A
  • each fiber innervated by ONE neuron at one location
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6
Q

what makes up a motor unit

A

one neuron can innervate many fibers (motor unit)

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7
Q

why do muscle fibers (cells) contain satellite cells

A

responsible for repair of muscle

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8
Q

what is excitation-contraction coupling

A

electrical stimulus (action potential) converted to mechanical response (contraction)

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9
Q

synaptic vesicles contain what neurotransmitter

A

acetylcholine (Ach)

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10
Q

active zone of neuromuscular junction

A

storage and release site for vesicles

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11
Q

motor endplate of neuromuscular junction

A

sarcolemma opposite to synaptic terminals; has receptors for Ach

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12
Q

What are Ach receptors at neuromuscular junction

A
  • mixed-cation channel (simultaneous Na+ and K+)
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13
Q

End Plate Potential (EPP) at neuromuscular junction

A
  • depolarizing graded potential that results from the opening of Ach receptors
  • EPP reaches threshold and initiates action potentials
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14
Q

characteristics of Motor end plate

A
  • portion of sarcolemma directly across from the synaptic terminal
  • Ion channels in motor end plate are chemically-gated (bind acetylcholine)
  • capable of End plate potential (EPP), NOT action potentials
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15
Q

characteristics of sarcolemma

A
  • plasma membrane of a muscle fiber
  • electrically similar to axonal plasma membranes
  • can propagate self-regenerating action potentials
  • action potentials due to voltage gated Na+ channels
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16
Q

What type of potential is localized to motor end plate

A

graded potential EPP

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17
Q

what causes 1 miniature end-plate potential (MEPP)

A

each vesicle release of Ach

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18
Q

1 vesicle contains how many Ach molecules?

A

1 quantum = 10,000 Ach molecules

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19
Q

Summation of multiple MEPPS (miniature end-plate potentials) produce what?

A

an EPP

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20
Q

what does the EPP magnitude depend on?

A

depends on the amount and duration of Ach at the end plate

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21
Q

List the steps of neuromuscular transmission from beginning (traveling AP) to diffusion of neurotransmitter to sarcolemma

A
  • Action potential arrives in presynaptic motorneuron axon terminal
  • opening of voltage-gated CALCIUM channels and entry of calcium into axon terminal
  • release of Ach from synaptic vesicles into synaptic cleft
  • diffusion of Ach to sarcolemma
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22
Q

what happens when Ach binds to Ach receptors on the motor end plate within sarcolemma

A
  • the conductance of the motor end plate to Na+ and K+ (predominantly Na+) increases
  • results in EPP
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23
Q

how is a action potential on sarcolemma initiated

A

depolarization of muscle membrane adjacent to motor end plate reaches threshold and opens voltage-gated channels which initiate AP on sarcolemma

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24
Q

action of acetylcholinesterase (AChE)

A

degradation of acetylcholine

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25
Q

how do synaptic vesicles get to the synaptic membrane

A

SNARE proteins

26
Q

what are the SNARE proteins

A
  • synaptobrevin
  • SNAP-25
  • Syntaxin
27
Q

binding of Ach to the receptor on the motor end plate allows for the channel to open to what?

A
  • Na + (goes in)
  • K+ (goes out)
28
Q

factors that can affect the magnitude of EPP

A
  • voltage-gated calcium channel function
  • amount of Ach release
  • rate of Ach breakdown
  • Ach receptor agonists and antagonist
29
Q

what is the margin of safety

A

difference between the size of the EPP and the size of the threshold stimulus necessary to evoke an AP

30
Q

normally, how many single motor neuron action potentials can cause a large enough EPP to initiate a muscle cell AP

A

a single motor neuron AP

31
Q

why is there a margin of safety

A
  • there is typically far more Ach (3x) released and receptors activated than needed for depolarization
  • ensures that muscles activate every time signal is sent
  • prevents catastrophic failure of neuromuscular transmission and provides a buffer to ensure every time
32
Q

where is acetylcholinesterase located

A
  • located in junctional gap and post-synaptic folds
  • rapidly degrades Ach
33
Q

Acetylcholinesterase breaks acetylcholine into what two molecules? What happens to them?

A
  • Acetate and choline
  • choline is returned to the synaptic knob where it is recycled and reformed with acetyl Co-A into Acetylcholine
34
Q

How does acetylcholine, synthesized in the synaptic knob (from acetyl Co-A and choline) get transported into the vesicles

A
  • via a second messenger ACh-H exchanger (ACh comes in and H+ leaves vesicle)
  • a ATP generated proton pump provides the H+ into the vesicle necessary for the ACh-H exchanger
35
Q

What is the Botulism toxin’s effect on SNARE proteins. How can this be harmful? How can this be beneficial?

A
  • causes degradation of SNARE proteins
  • prevents fusion of synaptic vesicles
  • causes: flaccid paralysis and death via respiratory paralysis
  • Used clinically to treat many conditions including muscle spasms
36
Q

What the mechanism of action of the drug Curare

A
  • competitive antagonist: competitively blocks binding of Ach to receptors
  • causes: paralysis
  • reversible
  • used during surgery as a adjunct to but not as a replacement for anesthesia
37
Q

What is the mechanism of action in the disease Myasthenia Gravis

A
  • circulating antibodies block Ach receptors and cause them to be endocytosed and degraded
  • EPP decreases
  • decreased margin of safety
  • recruitment declines with use; some motor units fail to reach threshold due to decreased margin of safety
38
Q

Why is Neostigmine used to treat Myasthenia Gravis

A
  • it is a reversible acetylcholinesterase inhibitor
  • prolongs and enhances action of ACh at motor end plate
39
Q

What is the mechanism of action of Hemicholinium

A
  • blocks reuptake of choline into presynaptic terminal
  • depletes ACh stores from presynaptic terminal
40
Q

The action potential travels through the entire sarcolemma and into what structure?

A

Transverse T-tubules

41
Q

where is calcium stored in the muscle

A

sarcoplasmic reticulum

42
Q

what is a triad?

A

proximity of the two sarcoplasmic reticulum membranes and a T-tubule

43
Q

T-tubles contain what type of calcium channels

A

slow-activating voltage-gated Ca2+ channels called DHP receptors in skeletal muscle

44
Q

The sarcoplasmic reticulum membrane contains what type of Ca2+ channels

A

Ca2+ release channels callled Ryanodine receptors (RYR)

45
Q

how is calcium released from the Sarcoplasmic reticulum

A
  • upon depolarization of the T-tubles, a conformational change occurs in the DHP receptor that mechanically opens the RYR on the SR
  • calcium is then releases from the SR
46
Q

function of calsequestrin (Casq)

A
  • calcium binding protein in the SR
  • allows the SR to store a large amt of calcium
  • keep free calcium concentration in SR low
47
Q

Malignant Hyperthermia

A
  • inherited syndrome: sensitive to anesthetics
  • gene mutation in RyR and calsequestrin or DHD receptor
  • Ca2+ channel of SR is abnormally sensitive to anesthetic
  • release of Ca2+ is uncoupled from sarcolemmal AP
  • skeletal muscles contract forcefully w/o AP
48
Q

treatment for malignant hyperthermia

A

dantrolene sodium

  • muscle relaxant that abolishes E-C coupling by acting on the RyR
49
Q

myosin and actin, which is thick and which in thin filament

A

myosin (thick)

actin (thin)

50
Q

composition of myosin filament

A
  • each myosin molecule is composed of two proteins twisted together forming a tail with two heads (Cross-bridge)
  • myosin has ATPase activity
51
Q

composition of actin filament

A

core of a single actin filament consists of many actin globular molecules (G-actin) as a two stranded helical structure

52
Q

role of Tropomyosin

A

inhibits binding of myosin to actin

53
Q

role of Troponin (Tn) (3 parts)

A

Ca2+ -sensitive molecular switch

  • TnC: calcium binding produces conformational change in Tnl
  • TnT: links Tn complex to tropomyosin
  • Tnl: binds to actin and inhibits myosine ATPase
54
Q

role of calcium in the regulation of myosin binding to actin

A
  • Ca2+ binding to troponin complex allows for physical repositioning of tropomyosin filament, which exposes the myosin binding site on the actin molecules
55
Q

sliding filament theory

A
  • contraction occurs by the sliding of thin filaments past thick filaments: sarcomere shortens
  • result: muscle shortening
  • contractile force produced by muscle iber is proportional to the number of myosin cross-bridge-actin interactions
56
Q

cross-bridge cycling: energized state

A
  • cytosolic Ca2+ low
  • myosin and actin: dissociated
  • myosin head holds ADP and Pi
  • binding site on actin is blocked by tm/tn complex
57
Q

list step that lead to myosin binding to actin from the AP

A
  1. AP causes release of Ca2+ from SR
  2. Ca2+ binds to Troponin C
  3. conformation shift in Tm/Tn complex
  4. exposure of myosin binding to actin
  5. myosin binds to actin
  6. Pi release initiates the “powerstroke”
58
Q

what goes on during the Powerstroke

A
  • myosin head shift causing filament to slide
  • ADP released
  • myosin remains bound to acting until new ATP binds
59
Q

how does myosin become re-energized

A
  1. ATP binds to myosin causes it to release actin
  2. ATP hydolyzed to ADP - Pi
  3. energy released is stored in conformational shift of myosin head back to energeized state
  4. next cross-bridge cycle can occur
60
Q

How is calcium removed from the ICF back into the sarcoplasmic reticulum

A

via sarcoplasmic reticulum Ca2+ ATPase (SERCA)

  • triggered by high concentrations of Ca2+
  • must occur quickly

Physiology (7 decks)

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