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NPB 101L > Lab 2 Prelab > Flashcards

Lab 2 Prelab Flashcards

1
Q

What comprises the largest group of tissues in the body? What percent of body weight does it account for?

A

Muscle accounts for approx 1/2 the body’s weight

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2
Q

What are skeletal muscle fibers? What are they comprised of?

A
  • Individual muscle cells that make up skeletal muscle

- Comprised of myofibrils

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3
Q

What cause striations? What do striations look like?

A
  • Thick and thin filaments cause striations

- Thick filaments(A bands) appear darker than thin filaments (I bands)

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4
Q

What are myofibrils composed of?

A

Thick filaments (myosin) and thin filaments (actin)

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5
Q

Each thick filament is surrounded by __?

A

6 thin filaments

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6
Q

Each thin filament is surrounded by __?

A

3 thick filaments

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7
Q

What is a sarcomere? Components?

A
  • The functional contractile unit of a skeletal muscle

- Bundle of thick and thin filaments comprising the area b/t two Z-lines

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8
Q

What do motor neurons do?

A

Branch to innervate many individual muscle fibers

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9
Q

What does a motor unit consist of?

A

Motor neuron + all of the fibers it innervates

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10
Q

Small vs. Large motor units?

A
  • Small motor units allow for very fine muscle control w/ small force (ex. eyes)
  • Large motor units are incapable of fine control, but are able to create larger amounts of tension (ex. leg muscles)
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11
Q

What is the Henneman Size Principle?

A

Physiologically, motor units are activated from smallest to largest

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12
Q

How does the Henneman Size principle differ during artificial stimulation?

A

Artificial, direct stimulation recruits in the opposite order (large first, small later)

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13
Q

List the steps of excitation-contraction coupling in skeletal muscle.

A
  1. AP initiated and propagates to motor neuron axon terminals
  2. Ca2+ enters axon terminals through voltage-gated channels
  3. Ca2+ entry triggers release of ACh from axon terminals
  4. ACh diffuses from axon terminals to motor end plate in muscle fiber
  5. ACh binds to nicotinic receptors on motor end plate –> increases their permeability to Na+ and K+
  6. More Na+ moves into the fiber at the motor end plate than K+ moves out –> depolarizes membrane –> produces end plate potential (EPP)
  7. Local currents depolarize the adjacent muscle cell plasma membrane to its threshold potential –> generates AP that propagates over muscle fiber surface and into fiber along T-tubules
  8. AP in T-tubules triggers release of Ca2+ from sarcoplasmic reticulum
  9. Ca2+ binds to troponin on thin filaments –> tropomyosin moves away from its blocking position and exposes cross-bridge binding site on actin
  10. Energized myosin cross bridges on thick filaments bind to actin
  11. Cross-bridge binding triggers release of ATP hydrolysis products from myosin –> produces angular movement of each cross bridge
  12. ATP binds to myosin –> breaks linkage b/t actin and myosin –> allows cross bridges to dissociate from actin
  13. ATP bound to myosin is split –> energizes the myosin cross bridge
  14. Cross bridges repeat steps 10-13 –> thin filaments slide past thick filaments –> movement continues as long as Ca2+ remains bound to troponin
  15. Cytosolic Ca2+ conc decreases as Ca2+ is actively transported into SR by Ca2+ -ATPase
  16. Removal of Ca2+ from troponin restores blocking action of tropomyosin –> cross bride cycle stops –> muscle fiber relaxes
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14
Q

What is the neuromuscular junction?

A

Area where the motor neuron synapses on the muscle fiber

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15
Q

What steps of excitation-contraction coupling occur at the NMJ?

A
  • Depolarization @ axon terminal causes opening of voltage-gated Ca2+ channels
  • Ca2+ entry and binding to vesicles promotes fusion and release of ACh into the synaptic cleft
  • ACh binds to nAChR on the muscle fiber, causing them to open
  • ACh reuptake channels refill axon terminal and end stimulation
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16
Q

What is the motor end plate?

A

Portion of the sarcolemma that is in contact w/ the presynaptic terminal

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17
Q

What occurs at the motor end plate?

A
  • ACh binding to nAChR opens its associated Na+ channel
  • Na+ entry causes a graded depolarization (EPSP or IPSP)
  • If enough depolarization occurs to reach threshold, nearby voltage-gated Na+/K+ channels open, triggering an AP that propagates along the muscle fiber
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18
Q

What is EPSP? IPSP?

A
  • EPSP = excitatory post synaptic potential

- IPSP = inhibitory post synaptic potential

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19
Q

What is nAChR?

A

Nicotinic ACh Receptors

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20
Q

What are T-tubules?

A

Transverse tubules: invaginations fo the plasma membrane

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21
Q

What is the function of the T-tubule?

A

Bring APs into the interior of skeletal muscle fibers –> spreads APs across a greater surface area of the cells

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22
Q

APs travel into the T-tubules alongside the __?

A

Sarcoplasmic Reticulum

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23
Q

What is DHPR? RyR?

A
  • DHPR: dihydropyridine receptor

- RyR: ryanodine receptor

24
Q

Where do DHPR and RyR sit?

A

At the boundary of the T-tubule and SR

25
Q

What steps of excitation-contraction coupling occur at the T-tubule?

A

Depolarization at the T-tubule opens voltage-gated DHPR –> RyR opens since it’s paired to DHPR –> allows Ca2+ efflux out of SR and into cytoplasm of muscle cell

26
Q

What does the troponin-tropomyosin complex do?

A

Inhibits cross bridge formation

27
Q

Describe actin-myosin cross bridging. How does it start? End?

A

Ca2+ binds to troponin –> pulls tropomyosin off myosin binding site –> allows cross bridges to form –> cycle of ATP hydrolysis ratchets myosin head along actin to contract muscle fiber –> contraction cycle ends when intracellular Ca2+ is no longer bound to troponin

28
Q

Define twitch. Cause?

A

Small muscle contraction caused by a single AP or by direct stimulation

29
Q

Temporal vs. Spatial summation

A
  • Temporal: higher stimulus frequencies –> increased tension as twitches begin to merge
  • Spatial: higher stimulus intensity –> increased motor unit recruitment and higher tension
30
Q

What does tension look like at low frequencies?

A

Single unfused twitches

31
Q

What causes tetanic contraction?

A

Max tension resulting in complete fusion of twitches

32
Q

What will be our passive tension for the frog muscle? Why is this important?

A

20g –> length-tension relationship

33
Q

Why is it important to keep the nerve and muscle moist w/ Ringers?

A

Cutaneous respiration

34
Q

What is synaptic transmission?

A

Process by which neurotransmitters are released by the presynaptic neuron, and bind to and activate the receptors of the postsynaptic neuron

35
Q

Define tetany.

A

SUMMATION OF TWITCHES = muscle fiber is stimulated so rapidly that it doesn’t have time to relax at all b/t stimuli, resulting in a maximal sustained contraction

36
Q

Isometric vs. Isotonic contraction.

A
  • Isometric: constant length

- Isotonic: constant force

37
Q

What is competitive inhibition?

A

A form of enzyme inhibition where binding of the inhibitor to the active site on the enzyme prevents binding of the substrate and vice versa

38
Q

During lab 2 (skeletal muscle), what nerve did we stimulate? This induced the contraction of what muscle?

A
  • Sciatic nerve

- Gastrocnemius muscle

39
Q

During lab 2 (skeletal muscle), what happened when the stimulus voltage was increased?

A

Spatial summation: increased motor unit recruitment and higher tension –> greater contraction

40
Q

During lab 2 (skeletal muscle), what happened when the stimulus frequency was increased?

A

Temporal summation: higher stimulus frequencies –> increased tension as twitches begin to merge –> tetany

41
Q

During lab 2 (skeletal muscle), what happened when we added tubocurare?

A

Muscle contractions decreased then eventually returned to normal

42
Q

During excitation-contraction coupling, Ca2+ triggers the release of ____ from the terminal button, and also binds to ____ in the sarcomere.

A
  • ACh

- Troponin

43
Q

Why is direct stimulation less efficient than neuronal stimulation?

A
  • Nerve stimulation activates many motor units, so many muscle fibers participate in contraction
  • Direct stimulation not as many muscle fibers participate in contraction (only the ones surrounding the site of stimulation)
44
Q

When the tibial nerve is stimulated at high voltage, peak response is reduced by APs called ____.

A

Antidromic APs

45
Q

Describe the shape of the voltage-tension curve w/ increasing voltage? Mechanism?

A

SPATIAL SUMMATION

  • steep at first b/c recruiting larger motor units first
  • flattens out at higher voltages b/c max recruitment of motor units
46
Q

Describe the shape of the frequency-tension curve w/ increasing frequency? Mechanism?

A

TEMPORAL SUMMATIOON

-starts at high point and increases

47
Q

Why does direct stimulation still work in the presence of tubocurare?

A

Direct stimulation bypasses NMJ where AChR is being blocked by tubocurare

48
Q

What are muscle cells?

A

Excitable cells that are able to develop tension

49
Q

What determines the size of a motor unit?

A

of muscle fibers it innervates

50
Q

Define EPP.

A

End Plate Potential: depolarization of the specialized muscle end plate

51
Q

Define MEPP. Sum of MEPPs?

A

Miniature End Plate Potential: smallest possible EPP; summate to produce an EPP

52
Q

What does direct stimulation bypass?

A

ACh pathway

53
Q

Threshold for direct vs. neuronal stimulation.

A

Direct stimulation has a higher threshold voltage than nerve stimulation

54
Q

When the tibial nerve is stimulated, what neurons fire APs?

A
  • Alpha motor neurons

- Sensory neurons

55
Q

What takes longer, an AP or a muscle contraction? How much longer?

A

Muscle contraction takes longer (~100x)

56
Q

What is responsible for the inherent frog HR seen even through there was no input from the CNS? What channels drive this autorhythmicity?

A
  • Pacemaker cells

- Funny channels

NPB 101L (13 decks)

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