Open AccessULTRASTRUCTURAL STUDY OF NEUROMUSCULAR JUNCTIONS IN EXPERIMENTAL AUTOIMMUNE MYASTHENIA GRAVIS (EAMG) IN RABBITS
Author(s) -
Aeizono Naoki,
Takeoka Osamu,
Hasegawa Michinori,
Yonezawa Takeshi,
Yamaguchi Kyohei
Publication year - 1985
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1985.tb00603.x
Subject(s) - myasthenia gravis , postsynaptic potential , neuromuscular junction , acetylcholine receptor , ultrastructure , subclinical infection , pathogenesis , pathology , acetylcholinesterase , lesion , medicine , thymectomy , cholinergic , sarcoplasm , anatomy , chemistry , receptor , immunology , biology , endocrinology , neuroscience , biochemistry , enzyme , calcium
Experimental autoimmune myasthenia gravis (EAMG) was produced in rabbits by the injection of acetylcholine receptor (AChR) protein from electric organ of Narkacion tokyonis with complete Freund's adjuvant, and the ultra‐structural alterations of the neuromuscular junctions were studied. A lesion comparable to human myasthenia gravis could be observed in these animals. In acute EAMG, which showed a rapidly progressive severe paralysis 19 to 24 days after the first inoculation, distinct degeneration of the postsynaptic membrane was observed. Sometimes an irregular gap was found between the nerve terminal and postsynaptic sarcoplasm. In chronic EAMG with mild and prolonged muscle weakness, which appeared 23 to 54 days after the first inoculation, poorly developed junctional folds with little degenerative change were seen. By a morphometric analysis, some of the changes were detected even in a subclinical EAMG. In the presynaptic region, there was no ultrastructural alteration except that an increase of nerve terminal area was observed in chronic and subclinical EAMG. The pathogenesis of these alterations was discussed. ACTA PATHOL. JPN. 35 : 621–629, 1985.