Acetylcholine is indeed the primary neurotransmitter at the neuromuscular junction (NMJ). It plays a crucial role in muscle contraction by facilitating communication between nerves and muscles. When an action potential reaches the end of a motor neuron, acetylcholine is released into the synaptic cleft (the gap between the neuron and muscle fiber).
This neurotransmitter then diffuses across the NMJ and binds to acetylcholine receptors on the post-synaptic sarcolemma (muscle cell membrane). This binding causes sodium (Na+) channels to open, allowing Na+ ions to flow into the muscle cell. The influx of Na+ ions depolarizes the sarcolemma, leading to the generation of an action potential in the muscle fiber.
It’s important to clarify that acetylcholine does not directly cause hyperpolarization; rather, it initiates depolarization. After the action is complete, acetylcholine is quickly broken down by the enzyme acetylcholinesterase, preventing continuous stimulation of the muscle. This systematic process is essential for controlled muscle contractions and movements.