Answer
The nerve signal (action potential) opens the calcium voltage gated channels in the synaptic knob. As a consequence, Ca++ ions enter the syaptic knob. Calcium induces the synaptic vesicles to release acetylcholine (ACH) into the synaptic cleft. ACH then diffuses across the synaptic cleft and binds with the acetylcholine receptors (ACHR) on the sarcolemma of the muscle end plate-- two ACH molecules bind to each membrane receptor. The membrane receptors are ligand (chemical) gated channels, and when the channels open, Na+ ions flow into to the cell; at the same time, but more slowly, K+ ions flow out of the cell through K+ ion gates that open after the Na+ gates. The flow of the Na+ ions down their electrochemical gradient depolarises the cell, and they continue to flow, reversing polarity from about -90 mV to about +50 mV and to as high as +75 mV at peak. Then the Na+ channels begin to close.
As the Na+ ion channels close and the outflow of K+ increases, the potential difference falls through +50 mV to zero ( depolarization) and on through resting polarization level to overshoot to hyperpolarization (-90mV). The resting membrane potential is slowly restored by the action of the Na+/K+ATPase pump.
Work Step by Step
The rapid changes in membrane potential from resting levels to depolarization, to peak positive voltage difference, and back to RMP and below is the end plate potential or EPP. The EPP is caused by the binding of the neurotransmitter to the ACH receptors. The EPP triggers the action potential that causes the muscle fiber to develop tension or contract.
