At the axon terminal of a motor neurone, an action potential arrives and triggers an influx of calcium ions. These calcium ions cause vesicles containing Acetylcholine (a neurotransmitter that works on cholinergic receptors) to fuse with the membrane and release their contents into the synaptic cleft. The ACh then binds to a receptor on the sarcolemma of the myocyte (muscle cell). This opens Na+ channels and causes an influx of sodium ions into the sarcolemma, therefore depolarising it and generating an action potential. This impulse travels down the T-tubules (invaginations of the cell membrane into the muscle cell) causing both an influx of calcium from the extracellular space and a release of calcium from the sarcoplasmic reticulum. This calcium binds to the troponin molecule on the actin thin filament, causing a conformational change which moves tropomyosin off the actin binding site. The myosin heads can now bind to the exposed actin filament and form a cross bridge. ATP binds to the myosin head and, in a series of steps involving ATP hydrolysis into ADP and Pi (inorganic phosphate), the myosin head performs a power stroke and pulls the actin filament closer to its M line. This shortens the length of the sarcomere and leads to muscle contraction.