How does excitation-contraction coupling proceed in skeletal muscle after acetylcholine binds its receptor?

• A. Troponin initiates AP propagation along T-tubules.
• B. End-plate potential triggers AP along sarcolemma and T-tubules; Ca2+ release from SR via ryanodine receptors triggers binding to troponin and cross-bridge cycling.
• C. End-plate potential triggers immediate cross-bridge cycling without Ca2+.
• D. Ca2+ influx directly from extracellular space only, no SR involvement.

Answer: (B)

Excitation-contraction coupling links the electrical signal from the motor neuron to muscle contraction. When acetylcholine binds receptors at the neuromuscular junction, it opens ligand-gated sodium channels and creates a local depolarization called the end-plate potential. If this depolarization is strong enough, it triggers an action potential that travels along the sarcolemma and into the T-tubules. The voltage change in the T-tubules activates the dihydropyridine receptors, which are mechanically connected to ryanodine receptors on the sarcoplasmic reticulum; this coupling causes calcium to be released from the SR into the cytosol. The increase in cytosolic Ca2+ binds to troponin C, prompting a shift in the troponin-tropomyosin complex that exposes actin’s myosin-binding sites. Myosin heads attach to actin and, using ATP, perform cross-bridge cycling to generate contraction. Relaxation occurs as Ca2+ is pumped back into the SR by SERCA pumps, lowering cytosolic Ca2+ and allowing tropomyosin to cover the binding sites again.