Bsf Exam 2: Skeletal Muscle Physiology

Front 1

what are the two main "players" in skeletal muscle contraction?

Back 1

Myosin and Actin

Front 2

What 3 things regulate skeletal muscle?

Back 2

Troponin
Tropomyosin
Ca2+

Front 3

What is the function of the alkali light chain on the myosin heavy chain?

Back 3

alkali stabilizes myosin head
and
regulates myosin ATPase activity

Front 4

What holds myosin in place?

Back 4

titin
(anchored at z and m lines)

-largest protein identified in nature
-fx in control of myosin assembly, muscle elasticity, and generation of passive tension

Front 5

What holds actin in place?

Back 5

nebulin

-helps keep actin aligned and determines length of sarcomere

Front 6

In the absence of ATP, what is the state of skeletal muscle?

Back 6

contracted

Front 7

What are the 5 steps of muscle contraction?

Back 7

1. ATP binds myosin head: actin & myosin dissociate
2. ATP hydrolysis (myosin ATPase)
3. Cross-bridge formation: myosin binds actin at new site (if enough Ca2+ present in cytosol)
4. Release of P from myosin: power stroke occurs
5. ADP release
(muscle will contract as long as Ca2+ is present, need repetitive action potentials for this)

Front 8

Rigor mortis is caused by what?

Back 8

loss of ATP which is required to release myosin actin cross bridge leading to rigidity

Front 9

muscle membrane potential is....

the activation threshold for the membrane is......

Back 9

-90mV

-55mV
(larger stimulus required than for neuron AP)

Front 10

How does a muscle action potential differ from a neural action potential (3 ways)?

Back 10

-resting potential is more neg
-duration of action potential is longer
-velocity of conduction is slower

Front 11

How does excitation of skeletal muscle occur?

Back 11

-an action potential in the motor-neuron in the anterior horn of the spinal cord releases ACh into neuromuscular junction/motor-end plate
-ACh binds a nicotinic receptor on an ion channel and the membrane of the skeletal muscle fiber becomes permeable to Na+ and K+ leading to depolarization
-local end-plate potential is created

Front 12

How is a signal terminated (2 steps) ?

Back 12

1. hydrolysis of ACh by ACHe and re-uptake into pre-synaptic terminal
2. diffusion of ACh away from synapse

Front 13

AChE hydrolyzes Ach into what 2 things?

Back 13

choline and acetate
(2-step process, choline then acetate released)

*choline used for re-synthesis of ACh

Front 14

DHRP (dihydropyridine) is on the (SR/T-Tubule). What is mechanically coupled to DHPR?

Back 14

DHRP is a voltage sensor "L-type" Ca2+ channel on the t-tubule
(4 DHRPs make a tetrad on T tubule faces)

RyR is mechanically coupled to the DHPR

Front 15

RyR (ryanodine receptor) is on the (SR/T-tubule). What happens to RyR when DHPR undergoes a conformational change?

Back 15

RyR is on the SR
(each RyR has 4 subunits that each bind a DHPR)

confirmational change on DHPR opens the RyR (Ca2+ release channel), it is "unplugged"
(when Ca2+ is higher in SR it allows it to move out into cystol)

Front 16

What are the 3 steps of calcium release from SR?

Back 16

1. membrane depolarization opens DHRP
2. DHRP causes RyR to open
3. Ca2+ exits SR via RyR and activates troponin C, leading to muscle contraction

Front 17

for muscle relaxation to occur what must happen?

Back 17

Calcium must be removed from cystol and pumped into SR via SERCA pumps (uses ATP)

(Calcium binds calsequestrin w/i SR)

Front 18

If an electrical stimulus is applied to a muscle, but no Calcium is present in cystol, will contraction still occur?

Back 18

yes, DHPR and RyR can initiate contraction with an electrical impulse, releasing calcium into cytosol, initial calcium presence not necessary

Front 19

Where are the 3 major sites that drugs effect to inhibit synaptic (neuromuscular) transmission?
give an example of each

Back 19

1. neuronal side of synapse
2. within synaptic cleft
3. on the postsynaptic membrane

Front 20

At the neuronal side of synapse what are 4 ways to effect signal transmission?

Back 20

1. block voltage-dependent Na+ channel
2. block voltage-gated K+ channel
3. bind and inhibit Ca2+ channel on nerve terminal
4. cleave key proteins involved in exocytosis

Front 21

Within the synaptic cleft, what are 2 ways to effect signal transmission?

Back 21

1. produce inactive AChE
2. inhibit enzyme

Front 22

At the postsynaptic membrane what are 3 ways to effect signal transmission?

Back 22

1. block voltage-dependent Na+ channel
2. bind nicotinic AChR
3. inhibit AChR receptor
(AChR agonist & antagonist)

Front 23

What 2 regulatory proteins are associated with F-actin?

Back 23

Troponin and tropomyosin

Front 24

In relaxed state, tropomyosin covers ____________________

Back 24

myosin binding site on actin

Front 25

What are the 3 units of the troponin complex and what do they do?

Back 25

Troponin T (TnT)- binds tropomyosin
Troponin I (TnI)- blocks myosin binding site on F-actin filament (inhibitory site)
Troponin C (TnC)- has 4 Ca2+ binding sites that regulate actin-myosin interaction (regulatory site)

Front 26

What is the triad made up of?

Back 26

1 T-tubule (penetrates deep into muscle)
2 sarcoplasmic reticulum cisternae (Ca2+ storehouse)
(one on each side of T tubule)

Front 27

Troponin C (TnC) has 4 Ca2+ binding sites, 2 high affinity and 2 low affinity, when the low affinity sites are bound what happens?

Back 27

TnI is moved away from actin
Tnt is pushed away from myosin binding site
--> this initiates muscle contraction via cross bridge cycling

Front 28

how does an action potential lead to contraction?

Back 28

action potential--> increased calicum--> muscle contraction