Lecture 17 & 18 Outline Flashcards

Question

Nerve muscle synapse is called...

Answer 1

neuromuscular junction (NMJ)

Answer 2

- from the primary motor cortex - send axons on the ipsilateral side - through brainstem on same side - then in the medulla oblongata, about 90% of those axons are going to cross over - make synapse on lower motor neuron, down in SC & that axon will exit through the ventral root & ultimately make a synapse on a muscle cell & cause contraction of that muscle

Answer 3

will control muscle cells on the left side of your body

Answer 4

a large number of muscle cells

Answer 5

EXCITATORY & uses n.t. ACh

Answer 6

is one motorneuron & all of the muscle cells it innervates

Answer 7

only one muscle cell, sometimes many

Answer 8

- motor neuron innervating only 1 muscle cell - 1 motor neuron is innervating a # of diff. muscle cells but still, each muscle cell receives only 1 synaptic input (more common)

Answer 9

neuromuscular junction (NMJ)

Answer 10

1. The NMJ is HUGE (1000 micrometers2) vs a central synapse (0.05 micrometers2) 2. The postsynaptic membrane is FOLDED & has a HIGH DENSITY OF nAChR (hundreds of thousands!!)

Answer 11

Central synapse: - SIMPLE! - 0.5 mV EPSP - has GPCR's & Ligand-gated ion channels NMJ: - NOT simple! - Folded to increase the SA! - High density of both nAChR (& the crests of these synaptic folds) & VG Na+ channels (fold in the trophs) - # of peaks & valleys (trophs & crests) & the NMJ - LARGE EPSP ~40mV

Answer 12

when the muscle cell; postsynaptic muscle cell sees this large EPSP, that's always enough to bring these VG Na+ channels to their threshold & they will fire an AP

Answer 13

1. The NMJ is HUGE (1000 micrometers2) vs a central synapse (0.05 micrometers2) 2. The postsynaptic membrane is FOLDED & has a HIGH DENSITY OF nAChR (hundreds of thousands!!) 3. The EPSP in muscle cell is LARGE (30-50 mV), whereas the EPSP at a central synapse may be 0.5-1 mV - b/c a lot of ACh binding to a lot of nAChR 4. High density of VG Na+ channels within the post synaptic folds

Answer 14

is that a single AP in a motor neuron will ALWAYS cause an AP in the postsynaptic muscle cell (no summation of EPSP) - HIGH SAFETY FACTOR! Described in more dets: - when there's an AP in a motor neuron, it releases ACh, it diffuses across the cleft & binds to the nicotinic ACh receptors on the muscle cell membrane - that causes a huge EPSP & that is always enough to cause an AP in that postsynaptic muscle cell - result of that: since there's an AP that always follows from the EPSP, we see that there's no summation of EPSP's at the NMJ - an AP will always result in contraction of that skeletal muscle (very special feature of neural muscular synapse) - has a very high safety factor

Answer 15

a number of muscle fibers (AKA muscle cells) lying parallel to one another and held together by connective tissue

Answer 16

elongated cells - multinuclear & generally lie the whole length of the muscle

Answer 17

muscle fiber

Answer 18

– Multinucleated – Large, elongated, and cylindrically shaped – Fibers usually extend entire length of muscle

Answer 19

very tough colajadece connective tissue

Answer 20

bundle of fibers - a bundle of muscle cells - all wrapped up to form this 1 single muscle

Answer 21

specialized endoplasmic reticulum for storing Ca++ ions thats found in muscle cells

Answer 22

1. Way its organized, it always sits in these certain positions, always sits with its middle here at the middle of the sacromere, & it extends

Answer 23

- imp. b/c they form a mesh network of canals & tubules that traverse all the way through the muscle - lie directly adjacent to the sarcoplasmic reticulum - - continuous with the sarcolemma itself

Answer 24

- membrane of the muscle cell | - basically just cell membrane of muscle cell

Answer 25

bundles of the contractile proteins

Answer 26

thick lines --> dark purple

Answer 27

thin lines --> light pink

Answer 28

so the dark & light bonds that make striated muscle have that unique appearance b/c of the presence of these thick & thin filaments

Answer 29

the sarcomere (goes from 1 Z-line (Z-disk) to another Z-line (Z-disk)

Answer 30

represents the length of those thick filaments

Answer 31

surround M line | - area where there are NONE of these myosin crossbridges

Answer 32

middle of sacromere

Answer 33

made up PRIMARILY just of myosin molecule

Answer 34

in middle of sarcomere

Answer 35

made up of this actin chain | - # of proteins come together to make this

Answer 36

on each side or end of sacromere

Answer 37

Protein molecule consisting of two identical subunits shaped like a golf club – Tail ends are intertwined around each other – Globular heads project out at one end

Answer 38

Tails oriented toward center of filament and globular heads protrude outward at regular intervals

Answer 39

cross bridges (molecular interactions) b/t thick & thin filaments

Answer 40

- An actin-binding site | - A myosin ATPase

Answer 41

actin, tropomyosin, troponin, nebulin, titin

Answer 42

G-actin monomers are spherical, but assemble into long chains

Answer 43

attachment with myosin head | - binding results in contraction of muscle fiber

Answer 44

regulatory proteins

Answer 45

Thread-like molecules that interacts with actin along its spiral groove

Answer 46

myosin binding sites

Answer 47

3 polypeptide units • One binds to tropomyosin • One binds to actin • One can bind with Ca2+

Answer 48

troponin stabilizes tropomyosin in blocking position over actin’s cross-bridge binding sites

Answer 49

tropomyosin moves away from blocking position With tropomyosin out of way, actin and myosin bind, interact at crossbridges Muscle contraction results

Answer 50

simultaneously combines with tropomyosin, actin & Ca2+

Answer 51

– Giant, elastic protein (1 of the largest proteins that we know of) – Joins M-lines to Z lines at opposite ends of sarcomere

Answer 52

• Helps stabilize position of thick filaments in relation to thin filaments - keeps thick filaments in the middle • Improves muscle’s elasticity - sarcomere can get longer & shorter; what titin does is it even looks like a spring & contributes to the elasticity of these proteins sliding past each other)

Answer 53

- aligns actin filaments

Answer 54

- M-line - main protein here that forms the M-line - a structural element to keep those thick filaments at the regular stacings

Answer 55

Muscle shortens when actin and myosin slide past each other

Answer 56

stretched | - thick filaments barely overlapping on the thin filaments

Answer 57

the thick & thin filaments are gonna slide past each other - then we'll see a greater degree of overlap (sarcomere is going to shorten & that's causing greater degree of overlap b/t thick & thin filaments)

Answer 58

- myosin head cocked (ready-in position) - tropomyosin partially blocks binding sites on actin - myosin is weakly bound to actin no Ca2+ ions

Answer 59

a calcium signal initiates contraction 1. Ca2+ levels increase in cytosol 2. Ca2+ binds to troponin (TN) 3. Troponin-Ca2+ complex pulls tropomyosin away from actin's myosin-binding site 4. Myosin binds strongly to actin & completes power stroke 5. Actin filament moves

Answer 60

in the initiation of contraction it is starting to bend & it's pulling/moving the actin

Answer 61

BINDING Myosin cross bridge binds to actin molecule POWER STROKE Cross bridge bends, pulling thin myofilament inward DETACHMENT (Ca2+ concen. is going to lower again) Cross bridge detaches at end of power stroke & returns to original conformation BINDING Cross bridge binds to more distal actin molecules; cycle repeated - will eventually allow this to bind all the way to the very middle (2-line)

Answer 62

DO NOT CONTRACT | - only the sarcomere can contract

Answer 63

motor protein: a protein that hydrolyzes ATP to convert chemical energy to carry out mechanical work

Answer 64

TIGHT binding in the rigor state - myosin head is bound very tightly to the actin molecule 1. ATP binds to myosin. Myosin RELEASES actin 2. Myosin hydrolyzes (breaks down) ATP. Energy from ATP rotates the myosin head to the cocked position. Myosin binds WEAKLY to actin - ADP & Pi remain bound 3. Ca2+ signal. Power stroke begins when tropomyosin moves off the binding site 4. Myosin releases ADP at the end of the power stroke - actin filament moves toward M line - head swivels - myosin releases Pi ADP releases

Answer 65

sarcoplasmic reticulum (SR)

Answer 66

very high Ca2+ concentration

Answer 67

* SR has a powerful Ca++ ATPase transporter | * SR also has a Ca++ binding protein called Calsequestrin.

Answer 68

Uses ATP to pump Ca++ from cytoplasm into SR

Answer 69

Helps maintain high Ca++ concentration

Answer 70

perpendicular from surface of muscle cell membrane into | central portions of the muscle fiber

Answer 71

edges of the A band (thick filaments, myosin)

Answer 72

surface membrane – action potential on surface | membrane also invade T-tubule

Answer 73

release of Ca2+ from SARCOPLASMIC RETICULUM into cytosol | - when it's in the cytoplasm of the muscle cell - that's when it will be free to interact with the tryponin

Answer 74

called this b/c their blocked by a class of drugs called dihydropyridine

Answer 75

b/c its blocked by a drug called ryanodine

Answer 76

PHYSICALLY connected by part of the ryanodine receptor called the foot

Answer 77

b/c its a big piece of globular protein & it literally interacts with this VG Ca2+ channel

Answer 78

1. We have an AP & it's traveling along the membrane of that muscle cell & it travels into the t-tubules of that muscle cell 2. As it travels into those t-tubules its gonna depolarize the membrane, & this is a VG Ca2+ channel so when it depolarizes it will open - so the depolarization causes the VG Ca2+ channel to open 3. Immediately what happens is a little bit of Ca2+ will enter the cytoplasm of that muscle cell 4. As this channel opens, its connected to the foot of the ryanodine receptor, & that physically pulls open the ryanodine receptor (it's a Ca2+ release channel) 5. When this ryanodine receptor opens, its going to allow a flood of Ca2+ into the cytoplasm of that muscle cell

Answer 79

1. An AP invades the presynaptic terminal and causes release of ACh 2. ACh binds to the receptor, allows entry of Na+, causes EPSP large enough to trigger an AP 3. The AP invades the T-tubule system 4. The AP causes the DHP receptor to open, and in turn, open the RyR channel. This causes a massive release of Ca++, and increase in intercellular Ca++ concentration 5. Ca++ binds troponin. Troponin pulls tropomyosin away from the myosin binding site on the actin protein 6. Power stroke 7. Actin filaments slide towards centre of the sarcomere 8. Free Ca++ pumped back into SR

Answer 80

• ~3-4 hours after death, peak at ~12 hours - muscle starts to become stiff * After death, intracellular Ca++ rises (leaks out of SR) * Ca++ allows troponin-tropomysin complex to move aside and allow myosin cross bridges to bind to actin. • But…. – ATP is needed to separate myosin from actin. – Dead cells don’t produce more ATP. – So once bound, cross bridges can’t detach. • Rigor mortis subsides when enzymes start to break down myosin heads

Answer 81

• Action potentials stop arriving at NMJ • ACh dissociates from AChR, gets degraded • Ca++ ATPase pumps FREE Ca++ back into SR • Ca++ dissociates from troponin, pumped back into SR • Tropomyosin moves back into position, blocking cross bridge binding site (will block that site where the myosin & actin can form that very tight bond) • Muscle ceases to maintain tension • Actin and myosin (are free to) slip past each other – Pulled by titin – Pulled by antagonistic muscle

Answer 82

with some elastic properties that will actually tend to pull that sarcomere apart a bit

Answer 83

muscles will be pulled - stretched back out by the antagonist muscle

Answer 84

1. Splitting of ATP by myosin ATPase for power stroke - when muscles die, this is no longer able to keep happening (this will be to a state of rigor mortis) 2. Active transport of Ca2+ back into sarcoplasmic reticulum - once Ca2+ is released into the cytoplasm of that muscle cell (when that muscle no longer needs to contract) , we've got to pump that Ca2+ back into the SR & get ready for the next muscle contraction 3. Na+/K+ ATPase - imp. b/c neurons & muscle cells need to have a RMP if their gonna generate APs)

Answer 85

1. Stored ATP (very little stored) - just a couple of secs worth 2. Creatine phosphate - First energy storehouse tapped at onset of contractile activity 3. Oxidative phosphorylation - Takes place within muscle mitochondria if sufficient O2 is present 4. Glycolysis - Supports anaerobic (absence of O2) or high-intensity exercise

Answer 86

oxidative phosphorylation or glycolysis

Answer 87

* During times of rest when ATP demand is low, muscle stores energy in the form of creatine phosphate * First store of energy tapped to fuel muscle contraction. (technically after "stored ATP" but it runs out after a few secs) * Provides 4-5 times the energy of STORED ATP • Limited supply (only a few minutes) - of activity that can be fuelled by creatine phosphate

Answer 88

the substrate for an enzyme called creatine kinase

Answer 89

bidirectional - in times of rest, it's able to use ATP to phosphorylate creatine to give you this reserve of phosphate in the form of creatine phosphate - but when use of muscle begins & it starts to use up its ATP then the creatine kinase enzyme can work in reverse & it can phosphorylate an ADP from the creatine phosphate to generate ATP

Answer 90

1 reactant ATP & a 2nd reactant a molecule called creatine & it can transfer 1 of the P's from the ATP to the creatine & you end up with a creatine phosphate molecule - product is a creatine phosphate & an ADP

Answer 91

goes to the left slide 50

Answer 92

goes to the right ATP can be used for muscle contractions - & then the concentration of ATP gets low in the cell - that's gonna favour the creatine kinase enzyme to work in reverse, allow the transfer of the phosphate on the creatine phosphate back to the ADP & create ATP which can now be used for muscle contraction

Answer 93

the process that provides energy during light to moderate exercise – Uses stores of glycogen (polymer of glucose) in muscle (30 min) – Good yield of ATP (38 per glucose molecule) – Aerobic exercise (b/c its using O2) – Adequate supply of oxygen

Answer 94

– Increase ventilation (increase breathing rate) – Increase heart rate and force of contraction – Dilate skeletal (muscle) blood vessels All of these processes will provide an increase blood flow to provide increase O2

Answer 95

Primary source of ATP when oxygen supply is limited (during intense exercise) - blood can no longer supply the amount of O2 thats needed to fuel the activity of your muscles

Answer 96

• Rapid supply of ATP – (b/c) Only a few enzymes involved BUT • Very low ATP yield – Only 2 per glucose molecule (remember oxidative phosphorylation gets you 38) – (end up with production of) Lactic acid, acidifies muscle and contributes to fatigue • Duration of anaerobic glycolysis is limited

Answer 97

Pyschological & Peripheral

Answer 98

happens after you've been working hard & you say I just can't do it anymore - different from person to person - who has it in them to dig a little bit deeper to be able to push just a little bit harder to get to the finish line - differences in ELITE ATHLETES

Answer 99

for the rest of us plays a more immediate role ``` (physiologists not really sure which is the most important) – Decrease in release of ACh – Receptor desensitization – Changes in of muscle RMP – Impaired Ca++ release by SR – Intracellular pH of muscle – Others… ```

Answer 100

from those lower motor neurons with sustained activity

Answer 101

idea that when receptors are exposed to a n.t. or their ligand for a long period of time they can lower their affinity for that very ligand

Answer 102

if muscle is very active for a long period of time then it will be firing a lot of APs - EVENTUALLY over a long period of time you may see slight changes in extracellular K+ & if that happens then a little bit higher concen. of extracellular K+ in the ECF is gonna depolarize those cells & those changes in RMP can lead to inefficiencies in being able to contact the muscle

Answer 103

after a while maybe the ryanodine receptors won't be as effective at allowing that muscle flow of Ca2+ into the cytoplasm of muscle cell

Answer 104

remember anaerobic activity can generate lactic & that can lead to acidification of muscle

Answer 105

tells us that in this whole experimental setup, what we also got done is the muscle is basically glued in some sort of apparatus that when theirs an AP - we can measure the tension generated

Answer 106

- the tension that's generated by the muscle cell - there is a substantial lag from the AP to the actual generation of tension - that period of delay from the AP to when it starts to generate tension is the latent period - all those events take time & contribute to this

Answer 107

- stimulate it at a very low freq. - every 200 msec - muscle cell is gonna generate some tension, slight latency & then the muscle cell will relax (repeat)

Answer 108

- stimulated with a duration of 200 msec from 1st to 2nd - tension & relaxation but now for this 3rd stimulation (triangle) we'll do it a little sooner - stimulate that muscle cell before its completely relaxed - can generate tension before that single twitch has actually been allowed to relax

Answer 109

- we're stimulating time after time after time in a repetitive way before it gets a change to relax & eventually we're gonna stimulate until it gets this point of max tension - call it unfused tetanus b/c that muscle cell (that fiber) is getting to relax a little bit from 1 pulse to the next - unfused b/c this curve is not smooth

Answer 110

* the most tension that a muscle cell can generate - you would generate from this complete (fused) tetanus - curve is smooth * * the most force a motor unit can generate ** - we're gonna stimulate this muscle cell a lot faster - so fast that it never gets any of these little opportunities to start to relax, it's just gonna generate tension in this very smooth fashion

Answer 111

generation of maximal tension (out of a single muscle cell)

Answer 112

• Some think it takes several APs to increase intracellular Ca++ enough to saturate actin’s myosin binding sites • Some think intracellular Ca++ reaches its maximum (saturates) after first action potential. – Summation and Tetanus develop because SUSTAINED elevation of increased Ca++ allows greater exposure of actin binding sites and therefore maximizes interaction with myosin (effect is time dependent)

Answer 113

too much or too little overlap of thick & thin filaments in resting muscle results in decreased tension - the amount of tension that a muscle or muscle cell generate depends on its initial resting state

Answer 114

optimal resting length

Answer 115

as you push the sarcomere more & more together it's not empty space - lots of other proteins in there (titin - big protein that takes up space), so the more you scrunch or push together this sarcomere all those other molecules start to push against each other & when that starts to happen - then that's working against the generation of tension

Answer 116

- the muscle cell is not able to generate as much tension b/t theirs not as many myosin heads able to interact with the actin binding sites - E is the most extreme ex: if you stretch out muscle fibers so far that theres no interaction/overlap b/t the myosin heads & actin binding sites then it can't possibly generate any tension

Answer 117

fibre types grouped together (white meat, dark meat)

Answer 118

interspersed

Answer 119

– Slow twitch oxidative (=red muscle) – Fast twitch oxidative-glycolytic (=red muscle) – Fast twitch glycolytic (=white muscle) interspersed with each other

Answer 120

dark meat (=red muscle) white meat (=white muscle)

Answer 121

1. Slow twitch oxidative (slow fatigue resistant) 2. Fast oxidative-glycolytic (fast fatigue resistant) 3. Fast twitch glycolytic (fast fatigable)

Answer 122

• Small amounts of tension, slowly • Capable generating tension for long periods of time without running down energy stores • Large numbers of mitochondria • Small fibres • Well vascularized, Myoglobin (to facilitate oxygen transfer from blood)

Answer 123

* Generate a lot of tension, moderately fast * Somewhat resistant to fatigue * Moderate # of mitochondria * Fibres are larger than slow twitch

Answer 124

``` – White muscle – Generate the most tension – Fatigue rapidly – Few mitochondria (Anaerobic catabolism) – Fibres are larger than slow twitch ```

Answer 125

slower to generate their tension but their fatigue resistant & they can keep going for a long time - able to generate the same amount of tension - NO change in force up to an hour after we start this exp.

Answer 126

after just a couple stimulations, it already gets to its peak - can do both glycolidic & oxidative phosphorylation - can maintain its tension for a while (6 mins later) - but by 4-6 mins that tension is starting to decrease - pooped out 50 mins later

Answer 127

generate more tension, quickly but poop out really fast - reaches its peak force much sooner than either the other 2 - generate a max force for ~ 1 min of activity but then it poops out real fast - clearly very fatigable

Answer 128

of the same type

Answer 129

different fibre types may coexist side by side

Answer 130

it turns out that motor unit will only include fibres of the same type - motor unit is 1 motor neuron & all the muscle fibres that it innervates

Answer 131

it turns out that motor unit will only include fibres of the same type - motor unit is 1 motor neuron & all the muscle fibres that it innervates

Answer 132

slow type, fast type or the fatigue resistant type

Answer 133

all has to do with the order in which those muscle cells are gonna be recruited

Answer 134

• First Motor units recruited: – Smallest motorneurons – Slow twitch fatigue resistant (red; oxidative) - if you lift a light weight these are the ones that your gonna activate 1st – Each MU has only a few fibres - small, weak & generate tension very slowly • Next recruited – These motor neurons are slightly larger – Motor units that include fast fatigue resistant fibres • Last recruited – Fast fatigable (= fast twitch glycolytic, white muscle) - lifting a really heavy weight & you need more strength to be able to finish that curl – The largest MN, include most fibres • Size principle

Answer 135

size does matter for muscle fibre recruitment refers to the idea: that when you've got a muscle & its being tasked to do some work - theres 3 sites, 3 general sizes of MN's (small, med, large) - 1st to become activated are gonna be the smallest MN's & they innervate the slow twitch fatigue resistant fibres - the med size MN's that innervate the fast fatigue resistant fibres get recruited next - & the last ones only when you really need them are the largest MN's & if they innervate the fast twitch glycolytic muscle fibres

Lecture 17 & 18 Outline Flashcards

(165 cards)