ALPHA-BUNGAROTOXIN SENSITIZATION IN EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS

A mouse model of MG, termed experimental autoimmune myasthenia gravis (EAMG), can be obtained after immunization with Torpedo acetylcholine receptor (AChR). Although many studies have detailed the consequence o f AChR antibodies binding at the neuromuscular junction and the diffic ulty in obtaining obvious clinical signs, less attention has been focu sed on the possibility of amplifying the muscular block in order to di scriminate between immunized and healthy animals. In the present studi es we observe that a single inoculation of alpha-bungarotoxin (alpha-b gt) can amplify the neuromuscular block revealed by repetitive nerve s timulation, and induce in EAMG mice a stable muscular weakness state l asting for at least 169 hours instead of 95 hours in normal mice. This model could provide an excellent tool for evaluating drugs active on neuromuscular transmission.