The effects of experimental autoimmune myasthenia gravis (EAMG) on acetylcholinesterase (AChE) were investigated in diaphragms of adult female Lewis rats. Both total AChE activity per muscle and release of enzyme activity during a 3-h incubation in vitro were measured. Two groups of myasthenic animals were used. Acute EAMG was induced by intravenous injection 48 h earlier with a syngeneic monoclonal autoantibody against the nicotinic acetylcholine receptor (AChR) of rat skeletal muscle; age- and weight-matched controls received a monoclonal anti-AChR antibody nonreactive with mammalian muscle. Chronic EAMG was induced by immunization 4 weeks earlier with AChR purified from Torpedo electroplax; controls received only adjuvants. When preparations from rats with acute or chronic EAMG were compared with the appropriate controls, no statistically significant differences in content or release of AChE activity were detected. Neither was there any change in the relative amounts of the various molecular forms of AChE in samples from animals with chronic EAMG. We conclude that the structural and functional changes arising in EAMG are highly specific for the acetylcholine receptor and associated elements of the neuromuscular junction, but have little impact on the biology of AChE.
ASJC Scopus subject areas
- Developmental Neuroscience