An action potential on a motor axon reaches the axon terminal, causing acetylcholine to be released. It diffuses across the neuromuscular cleft in synaptic vesicles and binds with acetylcholine receptors on the motor end plate (acetylcholine is later broken down by acetylcholinesterase). This causes an end plate potential, which depolarises the sarcolemma (the membrane around the muscle). This then depolarises the T tubules, which are in direct contact with the sarcoplasmic reticulum (the membrane which surrounds each muscle fibre). This results in the Calcium channels in the sarcoplasmic reticulum (called ryanodine receptors) to open, releasing calcium ions. These calcium ions bind to troponin, which pulls the tropomyosin away from the myosin-binding site (as it was blocking it). This allows the myosin heads to bind to the actin filament with the help of ATP hydrolysis, and the heads slide along the actin filament binding to different binding-sites, shortening the muscle fibre each time. This is skeletal muscle contraction.
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