4a. Skeletal Muscle and Neuromuscular Junction (NMJ) Flashcards

(50 cards)

1
Q

motor unit

A

motor neuron and all the fibers that it innervates

direct innervation (no ganglia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

motor end plates

A

located at skeletal muscle membrane
synapse with motor nerve terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

motor neuron site of action potential

A

axon hillock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

tetrodotoxin

A

blocks Na+ channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

botulinum toxiun

A

cleaves SNARE proteins
decrease NT release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

physostigmine/neostigmine

A

blocks AChE
increases ACh at NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

curare
(d-tubocurarine)

A

competitive antagonist for ACh to bind to the AChR
less ACh able to bind
=muscle relaxant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

end plate potential

A

graded potential (20mV)
generated by stimulation causing a change in membrane potential

almost always triggers AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dihydropyridine receptor (DHPR)

A

functions as a voltage sensor in skeletal muscle
triggers intracellular Ca++ release from SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T- tubules inside charge

A

+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T-tubules outside charge

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

t tubules function

A

conduct AP into interior muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DHPRs activated by AP

A

results in physical contact w/RyR to release Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Calcium-Induced Calcium Release
(CICR)

A

Ca++ release by the action of Ca++ alone without simultaneous action of other activating processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Primary mechanism of Ca++ release

A
  • direct protein-protein interaction between the DHPR and RyR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ryanodine Receptor

A

responsible for Ca++ release from SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when DHPR connects w/RyR

A

Ca++ is released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Excitation-Contraction Coupling

A

DHPR connecting w/RyR to facilitate Ca++ release
increase intracellular Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

myosin head

A

attaches to actin
power stroke (hydrolysis products released)
binds to new ATP
detaches from actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

myosin chains

A

heavy chain
light chain (regulatory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Actin filaments

A

provide cells w/mechanical support and driving forces for movment

22
Q

Troponin C (TnC)

A

Ca++ binding subunit

(during excitation)

23
Q

Troponin

A

works w/tropomyosin to unblock active sites between myosin and actin
allows cross-bridge cycling
contraction of myofibrils for systole

24
Q

Tropomyosin

A

binds w/troponin to help position it on the actin molecule

prevents myosin from forming cross-bridges while in a resting state

25
actin
protein that interacts with myosin filaments to generate tension
26
Hydrolysis of ATP/Power Stroke
1. ATP binds to myosin head (Attached) - dissociation of actin-myosin complex for myosin to bind to ATP (RELEASED) 2. ATP is hydrolyzed - myosin heads return to resting conformation 3. cross-bridge forms - myosin head binds to new action position 4. Phosphate release - power stroke: filaments slide past each other 5. ADP released
27
During muscle contraction, what happens to the H zones and I/A bands
H zones shrink/narrow I band shrink/narrow A band does not change
28
sarcomere optimal overlap
produces optimal force
29
too much overlap
lower force
30
not enough overlap
lower force
31
AChE breaks down ACh into
Choline + Acetic Acid
32
choline acetyltransferase (ChAT)
converts choline and acetyl CoA into ACh
33
3 ways to terminate contraction-reuptake of Calcium
1. NCX (Na/Ca exchanger) 2. SERCA 3. Calsequestrin
34
Na+/Ca++ exchanger
secondary active transporter requires ATP pumps one ion down gradient and the other up gradient
35
Sarcoendoplasmic Reticulum Calcium ATPase (SERCA)
pump transports Ca++ from cytosol back into SR against concentration gradient after muscle contraction primary active transport requires ATP
36
Calsequestrin
major Ca++ binding protein in SR main Ca++ storage regulator of Ca++ release channels in skeletal/cardiac muscle
37
fiber summation
recruit additional motor units
38
frequency summation
of individual fibers
39
unfused tetanus
muscle fibers do not completely relax before next stimulus b/c they are being stimulated at at fast rate Ca++ not at highest level (can trigger more Ca++ release from SR) partial relaxation between twitches (partial summation)
40
fused tetanus
complete tetanus no relaxation period between muscle contractions Ca++ reached highest level (cannot trigger more Ca++ release from SR) (full summation)
41
muscle relaxants
depolarizing non depolarizing
42
depolarizing agent
succinylcholine (partial agonist)
43
succinylcholine mechanism
activates NAChR maintains depolarization (keep open) causes paralysis - muscle fatigue - ion conc gradient? stops breathing
44
non-depolarizing agent
d-tubocurarine (antagonist)
45
d-tubocurarine mechanism
blocks binding of receptor ACh cannot bind No conformational change of receptor No EPP No AP
46
Rhabdomyolysis
damaged muscle tissue releases its proteins and electrolytes into the blood
47
Rhabdo symptoms
reddish/brown urine muscle pain/weakness/fatigue
48
Rhabdo blood serum
high creatine kinase high potassium high myoglobin low Ca++
49
Rhabdo kidney damage
myoglobin is filtered out by the kidneys which causes damage to the kidneys
50
Myasthenia Gravis
autoimmune diease antibodies bind to nAChR weakening skeletal muscles