Acetylcholine receptor and thymus in experimental autoimmune myasthenia gravis and experimental myositis.

This study was attempted to obtain information about biological properties of junctional acetylcholine receptor (AChR) and extrajunctional AChR, and about nerve influences on muscles AChRs under the pathological conditions of experimental myasthenia and myositis. Experimental autoimmune myasthenia gravis (EAMG) was induced in Wistar rats by immunizations with AChR purified from the electric organ of Narke Japonica without using Freund's complete adjuvant experimental myositis by immunization with rat muscle extract depleted of AChR. Thirty-five days after the initial immunization, unilateral dissection of the ischiadic nerve was performed in all immunized rats. Contents of AChR in both hind limb muscles were measured by double immunoprecipitation assay method 15 days after the experimental denervation. In the control animals the amount of AChR extractable from innervated muscles was 2.7 +/- 0.5 (mean +/- s.d.) pmole/g muscle and increased about 10-fold 15 days after the denervation (30 +/- 7.9). In rats with EAMG, AChR contents was reduced in both denervated (1.1 +/- 1.0) and innervated muscles (1.3 +/- 0.9). In experimental myositis, the increase of muscle AChR was impaired in denervated muscles (2.4 +/- 0.6), but AChR contents was not reduced in innervated muscles (2.7 +/- 0.9). These results suggest that nerves may influence AChR metabolism, keeping numbers of AChR constant even in inflammatory condition. In addition, germinal centre formation in thymic medulla was detected in EAMG rats.