Open AccessTRANSPLACENTAL TRANSMISSION OF EXPERIMENTAL AUTOIMMUNE MYASTHENIA GRAVIS
Author(s) -
Abizono Naoki,
Yonezawa Takeshi,
Yamaguchi Kyohei,
Furukawa Shoei
Publication year - 1983
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.1440-1827.1983.tb00357.x
Subject(s) - myasthenia gravis , postsynaptic potential , acetylcholine receptor , antibody , titer , antibody titer , neuromuscular junction , radioimmunoassay , receptor , medicine , immunology , chemistry , endocrinology , pathology , biology , neuroscience
Using neonates born from experimental autoimmune myasthenic rabbits, the authors demonstrated antibodies to acetylcholine receptor (AChR) in the newborn sera. By radioimmunoassay, antibody titers of 1‐day‐old neonates were roughly one seventh to one ninth of the mothers. At 8 weeks postpartum, the antibody was no longer detectable. Ultrastructural observations of the intercostal muscles of the neonates revealed two types of changes. The first type was degenerative alterations in the postsynaptic membrane. The second type of change, which was morphometrically analyzed, was immaturity of postsynaptic membrane structure with underdeveloped secondary synaptic clefts. After 28 days postpartum, these changes were not visible, thereby indicating that the process is reversible as the antibody titer decreases. These results suggested the possibility that the antibody to AChR, transferred transplacental, arrested the development of postsynaptic structure, although reversible, by blocking of the receptor sites in the end‐plate.