Neuronal signaling in muscle contraction is triggered when an action potential reaches the neuromuscular junction. At this junction, acetylcholine (ACh) is the main neurotransmitter. Packaged in vesicles, ACh fuses with the neuron’s membrane and is released into the synaptic cleft. ACh diffuses toward the motor end plate and bind to the neurotransmitter receptor on it. The muscle fiber is then triggered to produce an action potential of its own that spreads through the muscle’s T-tubules. The sarcoplasmic reticulum in the muscle releases Ca+ into the cytosol through various ion channels. After the sarcoplasmic reticulum has released Ca+, the Ca+ binds to molecules of troponin. This binding undergoes a change in its shape and this induces the tropomyosin to do the same. Tropomyosin changes its shape slightly exposing myosin heads that bind to the actin filament. Myosin heads pivot, forcing the actin to slide against the myosin filament. This is called a power stroke. Before the end of the power stroke, ATP binds to the myosin heads and releases the actin filament. Hydrolyzation of the ATP occurs and it becomes ADP and Pi. The energy released from this is used to cock back the myosin, preparing it for another cycle. When the action potential stops, Ca+ is pumped back into the sarcoplasmic reticulum. The Ca+ ions that are bound to troponin are released and the myosin-binding site is hidden by the tropomyosin. Both filaments, actin and myosin, slide back to their original positions. The contraction is done and is prepared for another contraction. [continues]
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