How does a nerve impulse translate in to skeletal muscle action? How does striated muscle work? What happens to these muscle cells when they are not stimulated?
1. Nerve impulse (action potential) arrives at axon terminal of a motor neuron (efferent). A motor neuron can innervate up to a couple thousand muscle fibers.
2. Voltage-gated calcium channels open and Ca2+ flows into the neuron.
3. Neurotransmitter acetylcholine (ACh) is exocytosed via synaptic vesicles into the synaptic cleft of the neuromuscular junction (NMJ)
4. ACh crosses cleft via osmosis.
5. ACh binds with nicotinic receptors on motor end plate of muscle cell. Unbound ACh is immediately degraded by an enzyme, ending effect.
6. ACh binding triggers the opening of channels that let Na+ in and K+ out. More Na goes in than K goes out so muscle cell is depolarized. An AP spreads along the muscle fiber's membranes including T-tubules, depolarizing the inner portion of the muscle fiber.
7. AP moving thru T-tubules triggers release of Ca+ from sarcoplasmic reticulum.
8. Calcium binds to troponin C on actin-containing thin filaments of the myofibrils. Calcium that is not bound is immediately pumped back into the sarcoplasmic reticulum.
10. ATP binds to myosin. If the myosin was hanging onto an actin, this makes it let go.
11. Myosin acts as an ATPase, breaking ATP into ADP and inorganic PO3. The breakdown of ATP provides the energy to "cock" the myosin head.
12. Troponin binding to Ca+ frees up the tropomyosin, which is obstructing binding sites for myosin on the actin thin filament.
13. Cocked myosin binds to free actin triggering the power stroke: Myosin releases ADP and inorganic phosphate and the head bends back, pulling the Z-bands towards each other, shortening the sarcomere and the I-band. Each skeletal muscle myosin head moves 10-12 microns per power stroke.
12. After power stroke ATP binds myosin, allowing it to release actin and be in the weak binding state.
13. ATP "cocks" the myosin and is hydrolyzed to ADP.
14. Etc etc etc until either ATP or Ca++ runs out. When calcium is no longer present on the thin filament, the tropomyosin changes conformation and blocks binding sites.