Acetylcholinesterase activity of skeletal muscle in a non-immunogenic model for myasthenia gravis in rats

Myasthenia gravis is caused by an autoimmune attack to acetylcholine recept ors of skeletal muscle. Acetylcholine release from motor nerve terminals is upregulated in patients with myasthenia gravis and also in rat "myasthenic " models, dependent on the reduction of the number of acetylcholine recepto rs. This study addresses the question as to whether at "myasthenic" endplat es there are changes in the activity of acetylcholinesterase. To this end w e studied acetylcholinesterase activity in junctional and extrajunctional r egions of dilator naris, extensor digitorum longus, and hemidiaphragm muscl es from rats with alpha-bungarotoxin-induced myasthenia gravis. In all stud ied muscles from "myasthenic" rats there was no significant change of junct ional acetylcholinesterase activity. In contrast, in dilator naris and exte nsor digitorum longus muscles, there was a 60% and 30% increase of extrajun ctional acetylcholinesterase activity. There was no significant change in t he extrajunctional activity in hemidiaphragm muscles. Velocity sedimentatio n analysis revealed that the increase in extrajunctional activity in extens or digitorum longus muscles could be attributed to an increase of the activ ity of the G(4) form of acetylcholinesterase. Treatment of rats with 6.4 mu gh(-1) neostigmine bromide for 29 days had no influence on junctional and extrajunctional acetylcholinesterase activity of extensor digitorum longus muscles from rats with alpha-bungarotoxin-induced myasthenia gravis.