What is the role of acetylcholine receptor (AChR) molecules in the pathogenesis of myasthenia gravis (MG)?

Updated: Aug 27, 2018
  • Author: Abbas Jowkar, MD; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
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Answer

In the resting state, there is an intermittent release of ACh molecules across the primary synaptic cleft. The ACh molecules serve as ligands and bind to the AChR on the post-synaptic membrane. Two molecules of ACh bind to the alpha subunits of the AChR, and fuse with it. The bound AChR then undergoes a 3-dimensional conformational change in the central ion channel portion of the AChR (M2, alpha-helical) opening the funnel-shaped cation channel (whose inner wall is negatively charged). This opening is very brief (about 1 ms) resulting in influx of sodium ions while simultaneously allowing potassium efflux along its opposite concentration gradient. This results in brief depolarization of the muscle membrane only at the junctional region creating a post-synaptic non-propagating depolarization called miniature endplate potentials (MEPPs).


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