Immunofluorescence Analysis of Surface Acetylcholine Receptors on Muscle: Modulation by Auto-Antibodies
Although the etiology of myasthenia gravis (MG) remains unknown, recent advances have established that it is an organ-specific auto-immune disease in which antibodies and lymphocytes are specifically reactive with nicotinic acetylcholine receptors (AChR) of skeletal muscle (reviewed in Ref. 9). Autoimmunity to AChR can be induced experimentally by inoculating animals with AChR and adjuvants (20, 23). The syndrome experimental autoimmune myasthenia gravis (EAMG) has been induced in rats using as immunogen AChR from either eel electric organ (10)or syngeneic muscle (14). An acute phase of profound weakness often occurs early in the course of EAMG and is transient. Many muscle fibers during this phase show evidence of denervation: a) miniature endplate potentials (mepps) are not detected (8); b) nerve stimulation fails to elicit an end-plate potential, although muscle fibers respond normally to direct stimulation (8); and c) the ultrastructure of the nerve terminal is normal but the terminal is separated from the muscle fiber by mononuclear inflammatory cells which phagocytose the postsynaptic membrane (5). A human equivalent of the acute phase of EAMG has not yet been described. The chronic phase of EAMG in rats resembles spontaneously occurring MG in man by every criterion examined so far.
KeywordsAntigenic Determinant Electric Organ AChR Antibody Bright Patch High Density Patch
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