Neuromuscular junction

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A neuromuscular junction is a type of synapse; a gap between a motor neurone and the muscle end plate known as the synaptic cleft which is approximately 50 nm wide. At a neuromuscular junction an action potential passes from the presynaptic membrane to the postsynaptic membrane, also known as the junctional folds present on the muscle end plate. This is to allow the signal to pass from the neurone to the muscle endplate, which will result in the relaxation or the contraction of the muscle.

In order for this action potential to be passed on to the postsynaptic membrane several steps occur:

  1. An action potential (generated at the axon hillock) travels down the axon by saltatory conduction to reach the axon terminal. This causes the depolarisation of the presynaptic membrane, which results in the opening of the voltage-gated calcium channels.
  2. Calcium ions move through the presynaptic membrane (down their concentration gradient) and into the axon. This causes vesicles that contain the neurotransmitter acetylcholine (the most common neurotransmitter) to fuse with the presynaptic membrane. This influx of calcium ions is an example of facilitated diffusion while the release of the neurotransmitter is an example of exocytosis. At the neuromuscular junction, the electric signal is converted into a chemical signal whereby the acetylcholine acts as the signalling molecule.
  3. The neurotransmitter acetylcholine then diffuses across the synaptic cleft (which is less than 1 ms in width) and binds to specific receptor proteins on the postsynaptic membrane of the muscle end plate.
  4. The receptor protein is a ligand-gated sodium channel which then opens upon reception of the signal.
  5. The opening of the channel causes an influx of Sodium ions, which diffuse down their concentration gradient into the postsynaptic membrane. As well as this potassium ions also diffuse out of the postsynaptic membrane. This causes depolarisation within the muscle end plate, and the action potential continues. Due to the channels in the junctional fold being ligand-gated and not voltage-gated, the depolarisation is called an End Plate Potential (EPP) and not an action potential. An EPP can trigger action potentials deeper in the muscle.
  6. To close the ligand-gated sodium channels and stop the depolarisation of the muscle end plate, an enzyme called acetylcholinesterase binds to acetylcholine and breaks it down into choline and acetate. Choline is then taken up to be recycled by the presynaptic membrane.

The EPP (End Plate Potential) on the postsynaptic membrane reaches -15 mV. This value is halfway between the equilibrium potentials of the sodium and potassium ions. Importantly -15 mV is not a full depolarisation but is greater than the threshold potential (-55 mV) and hence can trigger an action potential within the junctional folds where voltage gated sodium channels exist. The action potential triggered in the membrane then lead to contraction of the muscles[1][2].

In addition to EPPs, Miniature End Plate Potentials (MEPPs) can occur. These are randomly occurring depolarisations at the muscle endplate and they are of approximate magnitude 0.5 mV. They only are present at this magnitude as it is the equivalent to one synaptic vesicle fusing to the presynaptic membrane, releasing its neurotransmitter (Acetylcholine) into the snyaptic cleft in discrete quantities. This shows that either all of the contents of the vesicle are released or nothing is. Many MEPPs can build up and result in a motor EPP[3]. They usually occur when neurones and muscles are in their resting state, this is because the Acetylcholine maintains the contractions. MEPPs usually last for around one to two milliseconds[4].


  1. Alberts, Johnson, Lewis, Raff, Roberts, Walter; Molecular Biology of the cell, fifth edition; page 687-688, Garland Science
  2. Boyle and Senior, Biology, Collins Advanced Science, second edition, pages 354-357
  3. Purves D, Augustine GJ, Fitzpatrick D (2001). Neuroscience. 2nd ed. Sunderland: Sinauer Associates. Quantal Transmission at Neuromuscular Synapses.
  4. Siegel GJ, Agranoff BW, Albers RW (1999). Basic NeurochemistMolecular, Cellular and Medical Aspects. 6th ed. Philadelphia: Lippincott-Raven. contraction of the skeletal muscle fibres

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