When acetylcholine is released at a synapse, some of it diffuses across the synaptic cleft and binds to ACh receptors on the postsynaptic membrane. The postsynaptic membrane of the motor end plate is highly folded. ACh receptors are on the crests of the folds, and voltage-gated cation channels are at the bottoms of the folds and in the surrounding muscle cell membrane (see Figure 44.11). The ACh receptors are gated channels that allow both Na⁺ and K⁺ to flow through, but since the electrochemical gradients favor a net influx of Na⁺, the response of the motor end plate to ACh is to depolarize. That graded potential reflects the number of receptors activated. If sufficient numbers of receptors are activated, the membrane depolarization spreads to the depths of the folds of the motor end plate membrane and to the surrounding muscle cell membrane, which contain voltage-gated Na⁺ channels.

The spreading depolarization of the motor end plate activates the voltage-gated Na⁺ channels and causes the firing of an AP. This AP is then conducted throughout the muscle cell’s system of membranes, causing the cell to contract. We will discuss the contraction of muscle cells in greater detail in Key Concept 47.1.

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How much neurotransmitter is enough? Neither a single ACh molecule nor the contents of an entire vesicle (about 10,000 ACh molecules) will bring the membrane of a muscle cell to threshold. However, a single AP in an axon terminal releases the contents of about 100 vesicles—more than enough to fire an AP in the muscle cell and cause it to contract.