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Muscle Contraction Overview for MCAT
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Clik here to view.Sacromere
- Thick = Myosin
- Thin = acTin, Troponin, Tropomyosin
- Z line - boundary of sacromere (striation of muscle)
- M line - Middle of sacromere
- I-band - thIn filaments
- H-zone - Think filament
- A-Band = entire overlap of thick and thin filament (distance initial = distance final)- During contaction final distance b/w Z, M, I, and H decreases
Excitation-Contraction Coupling
1. Action potential from brain causes release of Acetylcholine at neural muscular junction
2. ACH binds to receptor on muscle membrane, causing increased permeability of muscle membrane to Na+
3. Increased permeability to Na+ causes Action Potential to occur in muscle membrane
4. Action potential spreads over entire surface of muscle membrane, down into T- Tubules5. Action potential in t-tubules causes Ca++ to be released from vesicles on sarcoplasmic reticulum
6. Ca++ binds to Troponin, causing Tropomyosin to slide OFF active sites on Actin cross-bridge binding sites
7. Exposed actin sites bind to myosin cross bridges, which were previously energized by breaking ATP by Myosin ATPase
8. Binding of Actin and Myosin causes cross bridge to Bend, causing Actin to slide INward.9. ADP and Pi released from cross bridge
10. New ATP molecule attaches to Myosin ATPase breaking bond between Actin and cross bridge , so cross bridge returns to original conformation
11. ATP split which energizes cross bridge
12. Cross bridge binds to New Actin site and slides Actin even further inward
13. Continued action brings actin over Myosin, resulting in muscle contractionMuscle Relaxation
1. Brain ceases action potential down motor neuron
2. No more ACH is released
3. No more binding of ACH on muscle receptor causes no more action potentials
4. With no more action potentials, Ca++ is actively transported back into vesicles
5. As Ca++ drops in cytoplasm, Ca++ bound to Troponin falls OFF, and tropomyosin rolls back over actin sites
6. Actin slides back into original positionProblems at Neuromuscular Junction:
1. Nerve gas inhibits ACH esterase
2. Curare binds to ACH site
3. Myasthenia gravis—ACH receptor destroyed by immune system
4. Botulism—blocks release of ACH
5. Hypothermia—blocks release of ACH