Muscle contractions - molecular mechanisms (wk4)

Question 1

Describe the motor unit:

Answer 1

-The motor neuron sends information to the muscle fibres as an action potential and propagates across the fibres.
-Multiple impulses are sent to the muscles to contract
-Muscles can be turned ‘off’ except from reflexes, from not moving and so no electrical impulses are sent throughout the body
-The greater the communication to the muscles the greater the contraction can become (because of the summation)
-Muscle -> fascicles -> muscle fibres -> myofibrils -> thick and thin filaments

Question 2

Describe the neuromuscular junction:

Answer 2

The neuromuscular junction:
1. Motor neuron’s action potential arrives at the axon terminal -> (action potential) Depolarizes plasma membrane.
2. Opening Ca+2 (calcium) channels -> Ca+2 ions diffuse into axon terminal -> Ca+2 binds to proteins.
3. Synaptic vesicles release Ach. (acetylcholine) (acetylcholine can be used to block receptors)
4. Ach diffuses from axon terminal to motor end plate, binding to nicotinic receptors.
5. Bindings of Ach opens an ion channel -> Na and K+ pass through these channels (electrochemical gradient across plasma membrane means more Na+ (sodium) moves in than K+ out)
6. Local depolarization of the motor end plate
7. Muscle fibre action potential initiated.
8. Propagation (end plate potential) (through muscle fibres and then there is a release of calcium through the fibres)

Question 3

Describe excitation-contraction coupling:

Answer 3

-Excitation-contraction coupling -> The sequence of events by which an action potential in the plasma membrane activates the force-generating mechanisms
-Every action potential in a motor neuron normally produces an action potential in each muscle fibre in its motor unit (1:1 relationship)
-An action potential in a skeletal muscle fibre lasts 1 to 2ms and is over before signs of mechanical activity begin
-Action potential propagation. Resting potential -> balance between Na+ and K. Depolarization -> imbalance, more Na+ than K. REPOLARIZATION. For the action potential to propagate, it has to pass a specific threshold of -80 to -30.
-Mechanical activity following can action potential may last 100ms or more (depending on availability of intracellular Ca2+)
1. Relaxed muscle -> Low Ca2+. Cross-bridge cannot bind with Actin because Tropomyosin is covering the binding site. (Troponin holds tropomyosin over binding site)
2. Active muscle -> High Ca2+. Ca2+ binds to troponin, tropomyosin moves away from cross-bridge binding site and then Actin binds to cross-bridge

Question 4

Describe the role of Ca 2+ in skeletal muscle contractions:

Answer 4

-2 proteins are responsible for linking the membrane action potential with calcium release in the cell -> Dihydropyridine (DHP) receptor (on muscle membrane) – and Ryanodine receptor (sarcoplasmic reticulum) (release calcium towards muscle cell to promote muscle contraction)
-Removal of Ca2+ from the cytosol requires energy
1. Action potential propagated along muscle cell membrane and into T-tubules
2. Ca2+ released from terminal cisternae
3. Ca2+ binding to troponin removes blocking action of tropomyosin
4. Cross-bridges bind, rotate, and generate force
5. Ca2+ transported back into sarcoplasmic reticulum
6. Ca 2+ removal from troponin, restores tropomyosin blocking action

Question 5

Describe the overview of the sliding filament mechanism:

Answer 5

-Shortening of the muscle is the result of certain parts of the actin and myosin filament interacting with each other
-Typically, muscle shortening involves one end of the muscle remaining at a fixed position while the other end shortens toward it
-Myosin is stable and does not move, actin slides/rotates over

Question 6

Describe the cross-bridge cycle 4 stages (part of the sliding-filament model)

Answer 6

1. Energized myosin cross bridges on the thick filaments, bind to actin
2. Cross bridge binding triggers release of ATP hydrolysis products from myosin, producing angular movement
3. ATP bind to myosin, breaking link between actin and myosin, which leads to the cross-bridge to dissociate
4. ATP bound to myosin is split, energizing the myosin cross bridge
   -Rigour mortis -> Cross-bridge forms and becomes unable to detach with the use of ATP
   -The ATP helps to bind the myosin head to the actin and this has to be completed before a muscle contraction can occur
   -The cross-bridge cycles can continuously occur if the myosin heads and receptor sites are ‘open’ and not covered
   -ATPase -> An enzyme which determines the speed of ATP hydrolysis and resulting sarcomere shortening velocity