The membrane of the nerve terminal has a different assortment of ion channels: fewer sodium channels, several types of potassium channels, and, most important, voltage-dependent calcium channels. When an action potential arrives at the nerve terminal, it opens the calcium channels and calcium ions move from the extracellular fluid, where the concentration is about 2.5 mmol/L, into the nerve terminal. There, active pumping of calcium ions across the nerve membrane into intracellular organelles (especially the endoplasmic reticulum and the mitochondria) keeps the concentration at about 1 mmol/L. The sudden increase in intraterminal concentration of calcium ions is linked to the release of acetylcholine by exocytosis at the synaptic vesicle release sites. The acetylcholine binds to receptor molecules on the postsynaptic membrane, opening channels that permit the influx of sodium ions and efflux of potassium ions. The net effect is a depolarization of the muscle membrane and a triggering of the muscle action potential. The acetylcholine is then rapidly hydrolyzed by acetylcholinesterase (AChE) into choline and acetate. The choline is conserved by active uptake into the nerve terminal, where it is reconverted into acetylcholine by the enzyme choline acetyltransferase.