All skeletal muscle cells are relaxed until they receive a command to contract from nerve cells called motoneurones. Motoneurone cell bodies are in the spinal cord while the myeli-nated axons run to the muscle. The axon terminal of the motoneurone that controls the gastrocnemius muscle contains vesicles of the transmitter acetylcholine (Fig. 17.3). To press the foot down, action potentials travel from the spinal cord down the motoneurone axon to its terminal, opening voltage-gated calcium channels in the plasma membrane. Calcium ions pour in, raising their cytosolic concentration from 100 nmol liter-1 to 1 ^mol liter-1. The calcium torrent causes the synaptic vesicles containing acetylcholine to fuse with the plasma membrane, releasing the transmitter into the extracellular fluid.
Acetylcholine survives only 0.2 ms in the extracellular fluid since it is quickly hy-drolyzed into choline and acetate by the enzyme acetylcholinesterase. However, its target— the skeletal muscle cell—is only 100 nm away. It hits its mark before it is broken down and binds to the nicotinic acetylcholine receptors present in the plasma membrane of the skeletal muscle cell. These open, allowing both potassium and sodium ions to pass. There is no large electrochemical gradient for potassium, but sodium is at a high concentration in the extracellular fluid and rushes in, depolarizing the plasma membrane of the skeletal muscle cell. The plasma membrane of the skeletal muscle cell also contains voltage-gated sodium channels. When the flow of sodium ions through the nicotinic acetylcholine receptors depolarizes the plasma membrane to threshold, the skeletal muscle cell fires an action potential, which in turn causes release of calcium from the endoplasmic reticulum (page 348). The resulting increase of calcium concentration in the cytosol of the muscle cell causes it to contract (page 393).
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