Page 1243 - Veterinary Immunology, 10th Edition

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FIG. 37.10 The pathogenesis of myasthenia gravis. Destruction of
acetylcholine receptors prevents effective neuromuscular
transmission. Blockage of cholinesterase activity by
anticholinesterase drugs permits acetylcholine to accumulate and
so enhances neuromuscular transmission.

In adult dogs, however, the acetylcholine receptor deficiency is
due to autoantibodies. These IgG antibodies accelerate degradation

of the receptors, block their acetylcholine-binding sites, and trigger
complement-mediated damage. As a result, the number of
functional acetylcholine receptors is significantly reduced. Dogs
may also make autoantibodies against titin, an intracellular muscle
2+
protein, and the ryanodine receptor, a Ca release channel in
striated muscle.
In normal muscles, the binding of acetylcholine to its receptor
opens a sodium channel to produce a localized endplate potential.

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