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MSK exam 3 AP lower limb > Excitation Contraction Coupling > Flashcards

Excitation Contraction Coupling Flashcards

1
Q

Somatic motor neurons (what are they and where do their cell bodies sit?)

A

Voluntary or reflex control

Efferent neurons

cell bodies sit in the CNS (ventral horn of spinal cord)

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2
Q

how many motor neurons is 1 myofiber supplied by?

A

1

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3
Q

how many muscle cells doe s1 motor neuron axon innervate

A

a few or many individual muscle cells

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4
Q

what is a motor unit

A

1 motor neuron and all the muscle fibers it innervates

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5
Q

NMJ (neuromuscular junction)

A

specialized synapse between motor neuron and skeletal muscle fiber

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6
Q

what are the similarities between a synapse and a neuromuscular junction?

A

two excitable cells separated by a narrow cleft that prevents direct electrical activity between them

means of communication is via chemical messengers that are released by the Ca 2+ induced exocytosis of storage vesicles when AP reaches the terminal

via the crossing of a neurotransmitter, and binding of it, induces opening of specific channels in the membrane, permitting ionic movements that result in a graded potential (subthreshold changes in membrane potential)

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7
Q

what are the differences between a synapse vs. neuromuscular junction?

A

synapse is between two neurons and NMJ exist between a motor neuron and a skeletal muscle

whenever you have an AP at a motor neuron you will get an AP of the muscle fiber (one-to-one transmission) WHEREAS one AP is a presynaptic neuron cannot by itself bring about an AP in a postsynaptic neuron ONLY can have AP when summation of EPSP’s brings the membrane to threshold

A NMJ is ALWAYS excitatory VS. synapse which can be both excitatory or inhibitory

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8
Q

what is an active zone ?

A

dense spots over which synaptic vesicles are clustered (located right over secondary postsynaptic clefts between adjacent postjunctional folds)

waiting to release neurotransmitter

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9
Q

what are postjunctional folds?

A

extensive invaginations on postsynaptic membrane directly under nerve terminal (high concentration of receptors)

increases surface area of muscle plasma membrane

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10
Q

what is acetylcholinesterase

A

AChE high concentration associated with synaptic basal lamina (basement membrane)

TERMINATES SYNAPTIC TRANSMISSION after AP

hydrolyzes ACh–> choline and acetate

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11
Q

nicotinic acetylcholine receptors??

A

these are the receptors that are expressed in high density at crests of postjunctional folds

this is the receptor we will be dealing with in skeletal muscles

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12
Q

where are NT vesicles produced and how do they get to their destination?

A

motor neuron cell bodies in the spinal cord produce NT vesicles

fast axonal transport translocates vesicles to nerve terminal (microtubule-mediated process)

Vesicles for ACh travel down axon EMPTY but contain presynthesozed peptides/peptide precursors already inside

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13
Q

what does choline acetyltransferase do?

A

synthesizes ACh from choline and acetyl CoA

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14
Q

what is synaptobrevin?

A

aka V-snare

essential for transmitter release

forms complex with SNAP-25 and syntax in

helps drive vesicle fusion

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15
Q

what are SNAP-25 and syntaxin

A

presynaptic membrane proteins t-SNARES

located on the presynaptic membrane of nerve terminal

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16
Q

what is synaptotagmin

A

Ca2+ receptor of synaptic vesicles

this detects the rise in Ca2+ and triggers exocytosis of docked vesicles

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17
Q

what makes calcium come into the nerve terminal?

A

at the nerve terminal there are voltage gated calcium channels that respond to action potentials that have reached the nerve terminal

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18
Q

steps in vesicle fusion?

A

synaptobrevin coils around free ends of syntax in/snap25 and brings the vesicle closer to the presynaptic membrane

when Ca2+ influx comes in, synaptotagmin detects this

this triggers vesicle fusion and exocytosis

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19
Q

what do neurotoxins do? and what is their effect

A

interrupt process of ACh release by blocking the fusion of synaptic vesicles (b/c of their effects on t-snares and v-snares)

which leads to no signal being transmitted!

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20
Q

Tetanus toxin and Botulinum toxins B,D,F and G do what?

A

these are endoproteinases (neurotoxins) that digest synaptobrevin

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21
Q

what does botulinum toxins A and E do?

A

cleave SNAP-25

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22
Q

what does botulinum toxin C1 do?

A

cleaves syntaxin

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23
Q

what type of receptor is the acetylcholine receptor?

A

Ionotropic, nicotinic AChR channel

nonselective cation channel at motor neuron endplate

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24
Q

what is the ACh receptor permeable and NOT permeable to?

A

permeable to cations (Na, K, and Ca) (not specific)

(note current of Ca is small under physiological conditions and its contribution can be ignored)

NOT permeable to anions (Cl-)

WEAK ionic selectivity–> function is to raise Vm above threshold

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25
Q

what happens when Ach binds to its receptor?

A

graded potential

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26
Q

opening of AChR channel at the muscle end plate does what?

A

now have increased permeability to Na and K

result is increase in the normally low permeability of Na relative to K+ (because Na usually doesn’t contribute to the resting membrane potential)

Vm shifts to a value between Ek and ENa
End-Plate Potential

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27
Q

what is End-Plate potential

A

a type of GRADED POTENTIAL which is a decremental spread of current

is is produced by transient opening of AChR

it is an EPSP (increased Na+ conductance drives Vm of end-plate region more positive)

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28
Q

what are the normal physiological conditions of ACh and EndPlate potentials?

A

presynaptic motor nerve axon AP–> depolarizing postsynaptic EPP

EPP is approximately 40 mV more positive than resting Vm

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29
Q

how is the Neurotransmitter action removed?

A

AChe hydrolyzes ACh to choline and acetate

removes ACh from NMJ synaptic cleft

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30
Q

Review of events at NMJ

A

see your drawing

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31
Q

what is a myofibril?

A

contractile element

contains thick and thin filaments

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32
Q

what is the level of coupling and contraction?

A

it is at the level of the myofibril and its striations

actin/myosin

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33
Q

Sarcomere

A

Z line to Z line

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34
Q

what is the A band

A

myosin thick filaments overlap with actin

35
Q

what is the h zone

A

middle of the a band part of myosin where actin does not overlap

36
Q

what is the m line

A

extends vertically down center of A band

37
Q

what is the I band

A

part of actin not overlapping myosin (does not project into A band)

38
Q

what is the z line

A

thin filament attachment

39
Q

what parts of the sarcomere shorten during contraction?

A

H zone
I band

Sarcomere is shorter

40
Q

what are the thick filaments?

A

bipolar assembly of multiple myosin molecules

2 myosin heavy chains (MHC)
-each heavy chain has a Rod, Hinge and Head

2 alkali light chains

2 regulatory light chains

41
Q

what are the 2 important binding sites on the head of the myosin heavy chain?

A

Actin binding site (for cross bridge formation)

Myosin ATPase site (for binding and hydrolyzing ATP)

42
Q

each head of myosin heavy chains forms a complex with what?

A

2 light chains (1 alkali and 1 regulatory)

43
Q

alkali light chain does what?

A

essential role in stabilizing the myosin head region

44
Q

what does the regulatory light chain do?

A

regulates myosin ATPase activity

45
Q

F-actin?

A

backbone of the thin filament

it is double stranded polymer of actin molecules

associated with Tropomyosin and Troponin

46
Q

what are troponin and myosin

A

2 important regulatory actin binding proteins

47
Q

what is the important binding site of Actin?

A

myosin binding site

48
Q

what blocks the myosin binding site on actin at rest?

A

tropomyosin

49
Q

what does troponin interact with?

A

1 tropomyosin molecule and actin

50
Q

what does tropomyosin interact with?

A

7 actin monomers

51
Q

3 components of Troponin

A

T
C
I

52
Q

Troponin T function

A

binds to a single tropomyosin molecule

53
Q

troponin C function

A

binds to Ca

54
Q

troponin I function

A

binds to actin and inhibits contraction

55
Q

titin does what?

A

tethered from M line to Z line

contributing to force transmission

involved in elastic behavior of muscle by maintaining the resting length of muscle during relaxation (passive stiffness)

56
Q

what is excitation-contraction coupling ?

A

process by which electrical excitation of the surface membrane triggers an increase of Ca2+

57
Q

what do AP’s propagate along?

A

from sarcolemma to the interior of muscle fibers along the transverse tubule network! Transverse t-tubules

58
Q

what does a depolarization of the sarcolemmal membrane result in?

A

rise in Ca2+ inside cell

59
Q

what is the location of the T-tubules in relation to the muscle fiber?

A

extend into the muscle fiber and surround the myofibrils at the junctions of the A and I bands

60
Q

where does intracellular calcium come from?

A

the sarcoplasmic reticulum

61
Q

what is the triad

A

T-tubule membrane and its 2 associated cisternae (specialized regions of sarcoplasmic reticulum)

propagation of AP into T-tubules depolarizes triad

results in Ca release from lateral sacs of the SR

62
Q

what is the function of the Dihydropyridine receptor?

A

DHP is a voltage gated channel located on the t=tubule membrane

it is the L-type Ca 2 channel

it induces a conformational change in the Ca release channel (RyR) by mechanical activation

63
Q

what is the RyR receptor

A

it is the Ca release channel located on the SR membrane that is facing the T-tuble

releases stored Ca from the SR

64
Q

what does the release of Ca into the muscle fiber do?

A

triggers contraction by removing inhibition of cross-bridge cycling

NOTE Ca does not directly interact with contractile proteins, but rather it’s role in contraction is through binding regulatory proteins

65
Q

in the presence of Ca what does troponin do?

A

removes tropomyosin from the myosin binding sites on actin

66
Q

what does mATPase do?

A

hydrolyzes ATP to ADP and Pi

creating potential energy

67
Q

what position are myosin head in at rest?

A

in the cocked position with stored potential energy

68
Q

what does the interaction between myosin and actin do

A

pulls the trigger using the stored potential energy

allows myosin to pull the actin toward the center of the sarcomere (power stroke)

sarcomere shortens

Pi is released from the cross bridge to trigger the power stroke

69
Q

when is ADP release

A

with the power stroke completion

70
Q

what must be present for multiple cross -bridge cycling to occur ?

A

ATP and Ca

71
Q

what are the steps in the cross bridge cycle?

A

1= atp binds to myosin head, causing the dissociation of the actin-myosin complex

2= atp is hydrolyzed causing myosin heads to return to their resting conformation

3-= a cross bridge forms and the myosin head binds to a new position on actin

4= pi is released, myosin heads change conformation resulting in the POWER STROKE
the filaments slide past eachother

5- ADP is released after power stroke, and the myosin/actin cross bridge remains in the tightened/shortned position

again ATp binds to the myosin causing dissociation

72
Q

what is rigor mortis

A

if their is no fresh ATP available such as after death, then actin and myosin remain bound in rigor complex

73
Q

what does ATP NOT Do

A

regulate the cross-bridge cycle of actin-myosin interaction

it will generally continue at physiological levles of ATP

74
Q

what is relaxation

A

requires reuptake of Ca from sarcoplasm AND ATP in order to dissociated myosin and actin from each other

it is an ACTIVE process (ca 2+ pumps and ATPase binding site on myosin head)

75
Q

what happens if reuptake is unregulated?

A

cross bridge cycling would continue until myocyte is depleted of ATP

76
Q

what happens when Ca 2+ levels inside the muscle cell decrease?

A

troponin and tropomyosin move back into place and cover myosin-binding site on actin

77
Q

what is the minor mechanism for Ca 2 removal from the cytoplasm?

A

Na-Ca2+ exchanger and Ca2+ pump

both extrude Ca+ across sarcolemma

78
Q

what is the major mechanism for Ca2+ removal from the cytoplasm?

A

sarcoplasmic and endoplasmic reticulum Ca2+-ATPase (SERCA) -type Ca2+ pump

79
Q

what inhibits activity of SERCA?

A

high Ca2+

80
Q

what is the function of Ca2+ binding proteins

A

delay inhibition of Ca2+ pump activity

they buffer increased Ca2+ during Ca2+ uptake and can increase the Ca2+ capacity of the SR

sort of take Ca out of the picture

can have up to 50 binding sites per molecule

81
Q

Calsequestrin

A

principal binding protein in skeletal muscle

localized in the SR beneath the triad junction

forms a complex with the Ca2+ release channel (RYR)

facilitates muscle relaxation by buffering Ca2+ and unloads its Ca2+ in the vicinity of the Ca2+ release channel to facilitate EC coupling

82
Q

Calreticulin

A

Ca2+ binding protein in smooth muscle

83
Q

look at the summary slides

A

do it

MSK exam 3 AP lower limb (15 decks)

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