What is the role of endplate potential (EPP) in the pathogenesis of myasthenia gravis (MG)?

Updated: Aug 27, 2018
  • Author: Abbas A Jowkar, MBBS; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL  more...
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ACh molecules bind to the AChRs resulting in a larger depolarization of the post-synaptic membrane resulting in the endplate potential (EPP). The amplitude of EPP is normally high enough to trigger an action potential at the post-synaptic membrane. The voltage-gated sodium channels present in the depths of the secondary synaptic cleft facilitate action potential, which is propagated along the NMJ muscle membrane. When this action potential invades the transverse tubule system of the muscle, another voltage-gated calcium channel (VGCC) becomes activated causing influx of calcium ions, and triggering mechanical contraction of the muscle fiber contractile apparatus.

The action of ACh on the post-synaptic membrane is short-lived and is terminated within a few milliseconds of its release from the nerve terminal through hydrolysis by the enzyme acetylcholinesterase into acetic acid and choline. The latter is taken up by the presynaptic membrane and repackaged into new ACh molecules.

The calcium ions are normally pumped out of the terminal portion of the axon within 100 ms, so they linger for a while and maintain the axon terminal in a hyperexcitable state, enhancing the release of ACh should a second action potential depolarizes the axon within this time frame.

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