What is the role of voltage-gated calcium channels (VGCCs) 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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The normal muscle fiber resting membrane potential is -80 mV (negative inside). The threshold for triggering an action potential in the muscle fiber is -50mV to -65mV. When a nerve action potential depolarizes the terminal axons, sodium ion conductance is increased and at the same time voltage-gated calcium channels (VGCCs) are activated, allowing an influx of calcium ion at the terminal portion of the axon. The entry of calcium ions is critical to the process of neuromuscular transmission (if Ca++ is removed from the extracellular space, NMJ transmission ceases). The entry of Ca++ starts a complicated interaction of many proteins including SNARE protein complex at the nerve terminal leading to facilitation of fusion of the ACh-containing vesicles with the presynaptic membrane. Consequently, the discharge of ACh occurs by exocytosis into the synaptic cleft. The greater the calcium concentration inside the presynaptic terminal, the more quanta of ACh are released into the synaptic cleft.

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