Chapter 9 & 10 (Muscle)

Question 1

muscle functional unit

Answer 1

sarcomere

Question 2

muscle is striated because of various sarcomeres

Question 3

z discs

Answer 3

delineated the boundaries of sarcomere

Question 4

I band

Answer 4

area on other side of z discs of other sarcomeres (thin and tighten filaments) (actin)
- thin filaments tethered to z discs
- thick filaments tethered to z discs through the elastic filament, titin (anchor myosin to z disc)

Question 5

M line

Answer 5

dissecting through thick filaments (myosin)
- tethered together by accessory linkages

Question 6

myosin head

Answer 6

enzymes must be bound to thick or thin filaments

Question 7

H zone

Answer 7

thick myosin filaments only
- immediately on the other side of the M line
- not tethered with accessory proteins

Question 8

thick filaments that have myosin heads have ATPases and thin actin filaments which have to binding sites for myosin heads

Answer 8

when they are bound they are going to involve ATP activity

Question 9

A band

Answer 9

on other side of the M line
- thick and thin filaments
- where power stroke takes place
- true functional unit

Question 10

muscle contractions (shorten)

Answer 10

z discs pulled closer together

Question 11

tropomyosin

Answer 11

long rope filaments that cover the active site on the actin (thin)
- prevents binding from thick to active only when tropomyosin moves out of the way to initiate power stroke

Question 12

troponin

Answer 12

kinda like gatekeeper
- moves tropomyosin out of way to expose actin thin filament binding sites for myosin ATPase
- responsive to calcium
- has calmodulin, binds calcium and initiates an activity

Question 13

need ATP to initiate power stroke and relieve the myosin heads from the thin actin filament binding sites

Question 14

rigor mortis (mort=death)

Answer 14

contracting of the muscles after death
- lack ATP for the hemolysis heads ATPase to hydrolyze the ATP and release itself from the actin sites
- do not have enough energy for myosin heads to break away from shorten contracted thin filaments
- condition

Question 15

rising intercellular calcium levels from t tubules responding to depolarization from a neuron
- neuron will depolarize and depolarization (generating electricity) travel down the cell membrane of the muscle
- electrical current will come from the neuron, the neuron will bridge at the neuromuscular junction from the neuron to the muscle cell
- that bridge is acetylcholine (to bridge the command from the brain and the neuron to the muscle)
- depolarization occurs on the cell membrane of the muscle
- t tubules (sarcoplasmic reticulum) will sense the electrical depolarization
- respond with voltage gated calcium channels, spill out calcium
- calcium goes out to calmodulin on troponin

Question 16

t tubules (sarcoplasmic reticulum)

Answer 16

modified smooth endoplasmic reticulums that sequester calcium, store calcium

Question 17

ON NEURON
- neuron depolarizes through voltage gated electrolight channels
- the act of the neuron depolarizing will activate on the neuron itself voltage gated calcium channels
- these channels are different from the neuron and muscle
- neuron channels once they sense depolarization they will open and allow influx of calcium extracellularly
- the action of calcium entering the neuron allows champagne bubbles which are vesicles filled with acetylcholine, receptors for motor neurons involved in initiating command for movement (contraction for muscle)
- when the vesicles filled with acetylcholine sense the rise for intercellular calcium they can then fuse to the cell membrane of the neuron of the neuromuscular junction and exocytosis the acetylcholine
- acetylcholine released into the neuromuscular junction, the synaptic cleft (where there is synapses of the neuron to the muscle), or motor endplate {all area where the nerve meets the neuron and through acetylcholine vesicles exocytosis ing)
- acetylcholine bridge the command between the nerve and the muscle
- acetylcholine carries the depolarization command from the nerve to the muscle

Question 18

synaptin

Answer 18

on the vesicle of the cell membrane of the neuron waiting to connect with a calcium ion and when it does it is going to dock the vesicle on the cell membrane of the neuron and it is going to drag it down until that vesicle will open up and that cell membrane will expand and it is going to allow the release of the acetylcholine into the neuromuscular junction
- arrive from the neuron to the surface of the muscle
- on the surface of the muscle acetylcholine is going to bind acetylcholine receptors
- allows the muscle to depolarize by opening the voltage gated sodium channels
- sodium is extracellularly with energy against its gradient and potassium is intercellular
- active transport is setting up this gradient
- acetylcholine is going to bind acetylcholine receptors
- sodium is rushing intracellularly with its gradient
- -90 to +30 rapid shift locally
- +30 is action potential
- bolt of electricity to the next area of the membrane that is at -90 because it will try to change it
- it will sense the voltage that arrived because of the gradient in charge from + to -
- opens another channel
- continues along the muscle membrane

Question 19

• nerve depolarization
• voltage gated calcium channels open up
• calcium enters
• binds synaptin
• synaptin docks the acetylcholine vesicles on the cell membrane of the neuron
• allows exocytosis of acetylcholine to neuromuscular junction

Question 20

REPOLARIZATION
- voltage gated sodium channels open up
- voltage gated potassium channels open up to neutralize
- potassium normally high intracellular and low extracellular will flow outwards
- potassium flows out of the cell extracellular and neutralize the charge back to -90 since positive ion is lost
- potassium will go with its gradient
- at this point high intracellular sodium and high extracellular potassium
- normally sodium is pumped outside and potassium inside against gradient (high extracellular sodium and high intracellular potassium)
- action potential is generated
- t tubules sense depolarization
- when it senses it is going to open up its voltage gated calcium channel, inside the myosite
- calcium released intracellularly in the myosite
- calcium rises in the myosite, goes right to calmodulin in the troponin, bind it
- troponin moves the tropomyosin (gate) out of the way
- move the tropomyosin filaments out from the actin binding sites, expose them
- myosin head ATPases can bind to the actin
- initiate ATPase activity
- draw the thin filaments towards the m line thus bringing the z discs together, shortening sarcomere, contraction

Question 21

the act of sodium flowing with its gradient into the voltage gated sodium channel and the act of potassium flowing out of the cell through voltage gated potassium channel are examples of secondary active transport

Answer 21

they are taking advantage of the gradient set up by active transport, the sodium potassium pump

• so when they flow with their gradient through voltage gated channels, it is secondary active transport

Question 22

voltage gated channels are secondary active transport

Answer 22

sodium potassium pump is active transport

Question 23

t tubules - modified endoplasmic reticulum (smooth/sarcomatic)

Answer 23

sense depolarization, the charge of the membrane

Question 24

• the means to this end is the depolarization of the neuron to release acetylcholine, to depolarize the membrane through the voltage gated sodium channel on the muscle
• so the means is depolarizes the muscle
• the ends is t tubules sensing the depolarization and releasing calcium to expose the actin active sites on the thin filaments, to get the myosin to bind there
• end is the power stroke from the myosin ATPase
• power stroke is what shortens the muscle

Question 25

lambert eaton syndrome

Answer 25

autoantibodies (antibodies that attack us) against the voltage gated calcium channels on the neuron - if blocked we can never release acetylcholine vesicles because we can not dock them without calcium (synaptin will not allow it) (blocking first step of neuron depolarizing)

Question 26

myasthenia gravis

Answer 26

autoantibodies against the acetylcholine receptor so blocking at the muscle step - if block at nerve step it is lambert eaton syndrome, if block at acetylcholine receptor on the muscle it is myasthenia gravis - acetylcholine will be released from the nerve - treated mostly by acetylcholinesterase inhibitors - when acetylcholine binds we don't want it to be bound there to fatigue the muscle cause it will constantly depolarize it - so an enzyme next to the acetylcholine receptor called acetylcholinesterase hydrolyses acetylcholine, breaks the bonds between the acetylcholine and the acetylcholine receptor (it is normal as it is how the muscle relaxes to stop depolarization) - we want the acetylcholine to be bound in myasthenia gravis because we want to keep as much normal acetylcholine that is able to bind bound as much as possible because it is having to compete against antibodies - we block the acetylcholinesterase enzyme in myasthenia gravis and it will allow the acetylcholine that did bind to stay bound as much as possible so we can get the net effect - normally acetylcholinesterase is a poison but in this condition it is a cure because normal people are not having to compete with autoantibodies to bind their acetylcholine - at the motor m plate

Question 27

malignant hyperthermia

Question 28

succinylcholine

Answer 28

stimulate the muscle through the acetylcholine receptors and fatigue it, the muscle becomes paralyzed until it can recover - primary basis for anesthesia - resistant to acetylcholinesterase degradation to an extent has a longer half life than acetylcholine and it will be a depolarizing neuromuscular blocker, it depolarizes the muscle to the point where it is fatigued and paralyzed

Question 29

malignant hyperthermia

Answer 29

- mutations in the t tubules that sense the voltages that can be more sensitive - runaway effect that the muscle is an constant contraction and if it is an constant contraction energy is burning and temperature rises - similar to a car overheating - excessive thermoenergy - give dantrolene as treatment, a calcium channel blocker that will overcome this effect - if you block the calcium, it will not be bind to the calmodulin of the troponin and not get the contraction

Question 30

serratus anterior

Answer 30

long thoracic nerve - its association with breast surgery - the fact that it can be cut - it will paralyze the serratus anterior - 90 to 120 degrees - "I cannot lift my arm high enough to comb my hair" because the serratus anterior is cut or lost

Question 31

sciatic

Answer 31

- gluteus maximus and piriformis - Piriformis Syndrome is a condition in which the sciatic nerve bisects the piriformis muscle - association with lower back pain

Question 32

lumbar stenosis

Answer 32

Lumbar spinal stenosis is a narrowing of the spinal canal, compressing the nerves traveling through the lower back into the legs - lumbar vertebrae