Starting with the release of acetylcholine what are steps in muscle contraction?

The process of muscle contraction initiated by the release of acetylcholine (ACh) at the neuromuscular junction involves the following steps:

1. ACh Release: Action potential traveling along the motor neuron reaches the neuromuscular junction. This causes the release of acetylcholine (ACh) from the presynaptic membrane.

2. Binding of ACh to Nicotinic ACh Receptors: ACh diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) located on the motor end plate of the muscle fiber.

3. Generation of End-plate Potential (EPP): Binding of ACh to nAChRs opens ion channels, leading to an influx of sodium (Na+) and potassium (K+) ions. This depolarizes the muscle fiber's membrane causing end-plate potential (EPP).

4. Depolarization and Action Potential Generation: If the EPP reaches a sufficient threshold, it triggers an action potential (propagated electrical signal) on the muscle membrane.

5. Excitation-Contraction (EC) Coupling: The action potential travels along the transverse tubules (T-tubules) into the muscle fiber. T-tubules are membrane invaginations that run perpendicular to the muscle fiber's surface.

6. Calcium Release from Sarcoplasmic Reticulum: The action potential causes voltage-gated calcium (Ca2+) channels in the T-tubules to open. This leads to the release of calcium ions (Ca2+) from the sarcoplasmic reticulum (SR) into the cytoplasm.

7. Calcium Binding to Troponin: The increased intracellular Ca2+ concentration causes it to bind to troponin, a regulatory protein on the thin filament of the sarcomere (the basic unit of muscle contraction).

8. Power Stroke: The binding of Ca2+ to troponin initiates conformational changes that move the tropomyosin molecules on the thin filaments. This exposes the myosin-binding sites on the actin molecules.

9. Formation of Cross-bridges and Contraction: The heads of myosin molecules (thick filaments) form cross-bridges with the exposed myosin-binding sites on the actin (thin) filaments. This forms the actomyosin complex.

10. Sliding Filament Mechanism: Myosin heads undergo cyclical binding, power stroke (working stroke), and detachment from the actin filaments while utilizing energy from ATP hydrolysis. This sliding filament mechanism generates muscle contraction.

11. Relaxation: When the action potential ends, calcium ions are pumped back into the sarcoplasmic reticulum by calcium pumps, reducing the intracellular Ca2+ concentration. This leads to the detachment of Ca2+ from troponin, allowing the tropomyosin molecules to move back to their original positions, blocking the myosin-binding sites. The cross-bridges break and the muscle relaxes.