L27

Question 1

explain neuromuscular junction

Answer 1

-under nervous control, may be conscious
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-site of communication between motor neuron + muscle fibre
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specialised structures on muscle fibres to facilitate communicatio

Question 2

explain excitation-contraction (EC) coupling

Answer 2

-events that allow motor neurons to stimulate skeletal muscle contraction via COMMUNICATION between the motor neurons and skeletal muscle fibres
-first relies on action potentials to move along axon/surface of muscle fibre (ideal for long distance, rapid + self-generating)
-but once reach synapse, need to reply on chemical messengers (neurotransmitters) that are also rapid, but have CONTROL compared to action potentials when crossing the synapse
-also electrical signals only effective along cell membrane, chemical work in sarcoplasm

Question 3

explain the neuromuscular junction.

Answer 3

-is the area of synaptic cleft (includes pre-synaptic, synaptic, and post synaptic area)
-Ach released across cleft, trigger action potentials in motor end plate (post synaptic)
-synaptic terminals sit in motor end plates (which is the other side of the synaptic cleft)
-action potentials travel across sarcolemma, depolarising the T tubules (because more sodium outisde then in, brings in a positive charge that causes depolarisation, goes into T tubules, T tubules transfer it to the middle of the muscle)
-calcium (+DHP) channels are voltage gated L-type Ca2+ channels
-Ach has Ach activated sodium channels

Question 4

what is the process of EC coupling

Answer 4

-depolarisation caused by Ach triggers Ca+ release
-DHP receptors occur on T tubule
-depolarisation of T tubule activates the DHP receptors
-RYR receptors occur on SR membrane
-activates DHP receptors, activates RYR, causes RYR to release Ca2+ from SR
-elevated sarcosolic Ca2+ interacts with troponin complex on the thin filament to allow contraction

Question 5

explain ATP

Answer 5

-is a source of energy
-each myosin head has a ATP binding pocket containing an ATPase
-within the pocket, ATP is hydrolysed to ADP +Pi + energy, ADP + Pi stays bound to myosin head
-this re-cocks myosin head in its high energy conformation
-so myosin heads loaded with stored energy primed for contraction
-cross bridge cycling uses energy stored from ATP hydrolysis in the power stroke
- Pi is released immediately before the power stroke, while ADP is released immediately after the power stroke
-myosin heads still attached to actin following the power stroke
-binding fresh ATP to myosin head breaks the cross bridge
-hydrolysis of that same ATP to ADP + Pi + energy recocks myosin heads in their high energy conformation

Question 6

4 steps of sliding filament theory (the contraction cycle)

Answer 6

=applies to skeletal muscle + cardiac muscle, also occurs to smooth muscle but in a slightly different way

1) cross bridge formation
-myosin head attaches to actin, forming a cross bridge
-occurs when Ca2+ levels high + active sites on actin exposed because troponin C is saturated

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2) power stroke
-Pi generated from hydrolysis released to strengthen the bond
-initiates power stroke
myosin head pivots + bends as it pulls along the actin
-then ADP released after

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3) cross bridge detachment
- new ATP attaches to myosin head, the link between myosin + actin weakens, cross bridge detaches

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4) myosin heads reset
-ATP is split into ADP + Pi, myosin head is energised (re-cocking, cycle repeats)

Question 7

explain skeletal muscle relaxation

Answer 7

• requires ATP (need energy to trigger muscle relaxation too), to pump Ca2+ back into sarcoplasmic reticulum + detach and reset myosin head (covering active site on actin)
• Ach is rapidly degraded by AchE + recycyled
  -troponin-tropomyosin cover the active site on actin
  -cross bridges can no longer form

Question 8

explain rigor mortis

Answer 8

-Ca2+ leaks into sarcoplasm
-cross bridges form + muscle contracts
-but no ATP to trigger relaxation, so permanently contracted
-thats why leads to stiffness

Question 9

smooth vs skeletal muscle

Answer 9

smooth
- active site son actin are always UNblocked (no troponin complex), so need a different calcium sensor
-uses calmodulin as the calcium sensor
-activates myosin light chain kinase enzymes, get phosphorylated (controls strength, direction of head, and modulation), causes the polymerasation
-myosin is scattered, but polymerase into thick filaments that are able to form cross bridges when Ca2+ conc. increases
-is very energy efficient, because while still only needed 1 ATP per cross bridge cycle, cycle is slower, so can hold tension without as much ATP
-thin filaments attached to dense bodies on cell membrane + a network made of desmin proteins

skeletal
-z line + nebulin hold the thin filaments in position
-active site sonly available if Ca2+ levels high, and troponin complexes are moved
-myosin always in form of thick filament