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24 Cards in this Set

  • Front
  • Back
nerve signal arrives at synaptic knob, causing calcium channels to open & Ca2+ to enter
excitation
Ca2+ trigger exocytosis of synaptic vesicles which release ACh into synaptic cleft
excitation
ACh binds to receptors on motor end plate, allowing Na+ to enter muscle fiber & K+ to leave muscle fiber
excitation
movement of ions across the sarcolemma creates a muscle action potential
excitation
muscle action potential spreads throughthe T-tubules into the sarcoplasm
excitation-contraction coupling
calcium release channels into sarcoplasmic reticulum and Ca2+ diffuse into sarcoplasm
excitation-contraction coupling
calcium ions bind to troponin molecules on thin filaments causing them to change shape
excitation-contraction coupling
troponin-tropomyosin complex shifts to a new position exposing myosin binding sites on actin filament so cross bridges can form
excitation-contraction coupling
the sliding filament mechanism
contraction
thin actin filaments slide inward past thick myosin filaments causing sarcomere to shorten
contraction
ATP attaches to ATP binding site on myosin head
contraction
ATP is split my myosin ATPase to energize myosin head
contraction
cross bridge formed by myosin head attaching to actin
contraction
power stroke
contraction
myosin head shrivels towar center of sarcomere drawing thin filament past thick filament
contraction
2nd ATP attaches to ATP binding site on myosin head, allowing it to detatch from actin filament
contraction
myosin head forms new cross bridge further along thin filament to produce another power stroke
contraction
repeated over & over to shorten sarcomere as long as ATP and calcium are present
contraction
when nerve signals no longer arrive at NMJ, synaptic know stops releasing ACh so nerve signals aren't transferred to motor end plate and calcium channels close
relaxation
ACh broken into fragments by acetylcholinesterase
relaxation
CA2+ are actively transported out of sarcoplasm & back into scarcoplasmic reticulum where they bind to calsequestrin
relaxation
troponin-tropomyosin complex moves back into position to block myosin binding sites on actin
relaxation
riger mortis
relaxation
CA+ leaks into sarcoplasm & bind to troponin to initiate cross bridge formation
relaxation