Neuromuscular function and transmission

Abstract

Neuromuscular transmission occurs across the tiny 50 nm gap between an axon terminal and a skeletal muscle fibre at the end-plate region. An axon with its many terminal branches and connected muscle fibres forms a motor unit. A single axon terminal contains thousands of vesicles of the chemical transmitter acetylcholine. An axonal action potential increases axon terminal permeability to calcium and the resulting increase of free calcium ions above the resting concentration causes about 100 of the vesicles to release their transmitter into the gap. The end-plate region is folded to increase its surface area to about 3000 square micrometres. The acetylcholine released reacts with acetylcholine receptors situated at the crests of these folds. When the receptor has bound two acetylcholine molecules it changes its configuration to form a cation pore that allows sodium and potassium ions to move in and out of the muscle end-plate region. The combined activation of 30,000,000 receptors occurring at one end-plate causes the muscle membrane to depolarize at the muscle junction to about −10 mV, forming a localized end-plate potential. Acetylcholine is rapidly destroyed by the enzyme acetylcholinesterase, which allows the receptors and membrane of the end-plate to recover and respond to further neuronal action potentials. Since the localized end-plate potential is well in excess of the threshold stimulus required to generate a muscle action potential, as long as acetylcholine is being released by presynaptic action potentials, then postsynaptic muscle action potentials will be produced and result in a maintained contraction.