What initiates the end-plate potential at the neuromuscular junction?

• A. Acetylcholine binding to nicotinic ACh receptors on the sarcolemma
• B. Acetylcholinesterase breakdown of acetylcholine in the synaptic cleft
• C. Opening of voltage-gated potassium channels in the sarcolemma
• D. Release of calcium from transverse tubules

Answer: (A)

The end-plate potential starts when acetylcholine released from the motor neuron binds to nicotinic acetylcholine receptors on the muscle’s motor end plate. These receptors are ligand-gated ion channels; when acetylcholine binds, the channel opens and lets positively charged ions, mainly sodium, flow into the muscle cell (with some potassium leaving). This inward current depolarizes the sarcolemma at the end plate, producing the end-plate potential. If this depolarization is large enough, it triggers voltage-gated sodium channels nearby and an action potential travels across the muscle fiber to initiate contraction.

Acetylcholinesterase breaking down acetylcholine terminates the signal, so it doesn’t initiate the EPP. Opening potassium channels would counteract depolarization rather than start it, and calcium release from transverse tubules occurs after the action potential to drive contraction, not at the initiation of the end-plate potential.