Abstract
In rats immunized with purified acetylcholine receptor protein (AChRP) from Torpedo electroplax, a defect of neuromuscular transmission physiologically identical to that seen in myasthenia gravis developed. The most sensitive index of the neuromuscular blockage was miniature end-plate potential (MEPP) amplitude. As early as 24 hours after inoculation with AChRP, the thymus showed reactive changes that are probably nonspecific. Removal of the thymus before or within three days after immunization delayed, but did not prevent, development of reduced MEPP amplitude. Prednisolone given within 35 days after immunization produced reversal of MEPP reduction within 24 hours, but had no such immediate effect when given 15 days later. It is probable that prednisolone acted by reducing the immunologic responsiveness of the animals during the developing phase of the defect of neuromuscular transmission.
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