After stimulation with an action potential (1), the synaptic terminal of a motor neuron releases acetylcholine and ATP. (2) Acetylcholine activates receptors in the muscle, which spurs voltage-gated sodium channels to open, triggering an action potential in the muscle, which contracts. At the same time, ATP or ADP stimulates P2Y1 receptors (3), which causes calcium ions to be released from the endoplasmic reticulum of the terminal/perisynaptic Schwann cell (TPSC) (4). In response, perisynaptic potassium ions (K+) produced by the muscle and neuronal cells move into the TPSC (5). Regulation of perisynaptic potassium ions by TPSCs is thought to reduce the ions’ ability to inactivate voltage-gated sodium channels during repeated firing, thus reducing muscle fatigue.