Place these events in the correct order of occurrence in the muscle contraction: End plate potential triggers an action potential Transverse tubules convey action potentials into the interior of the muscle fiber Acetylcholine binds to receptors on the motor end plate Calcium is released from the sarcoplasmic reticulum Ligand-gated channels open leading to depolarization Calcium ions bind to troponin, which then moves tropomyosin

1. Acetylcholine binds to receptors on the motor end plate

2. Ligand-gated channels open leading to depolarization

3. End plate potential triggers an action potential  

4. Transverse tubules convey action potentials into the interior of the muscle fiber

5. Calcium is released from the sarcoplasmic reticulum

6. Calcium ions bind to troponin, which then moves tropomyosin

Explanation:

Acetylcholine (ACh) is a signaling molecule (neurotransmitter) that binds to receptors on muscle cells. This binding triggers the opening of ligand-gated sodium channels, thereby ions enter into muscle cells, which causes the depolarization of the sarcolemma and thus promotes the release of Ca2+ ions from the sarcoplasmic reticulum. The myoneural junction, also known as the motor endplate, is the site of synaptic contact between a motor axon and a skeletal muscle fiber. The endplate potential is the voltage that produces the depolarization of muscle fibers when ACh molecules bind to their receptors in the cell membrane. This depolarization spreads in the sarcolemma through transverse tubules (T tubules​) and thus generates an action potential. Finally, this action potential induces the release of Ca2+ in the sarcoplasmic reticulum, which activates troponin protein and induces muscle contraction.

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