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 of AChR antibodies binding at the neuromuscular junction and the difficulty in obtaining obvious clinical signs, less attention has been focused on the possibility of amplifying the muscular block in order to discriminate between immunized and healthy animals. In the present studies we observe that a single inoculation of alpha-bungarotoxin (alpha-bgt) can amplify the neuromuscular block revealed by repetitive nerve stimulation, and induce in EAMG mice a stable muscular weakness state lasting 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.
Université Louis Pasteur, Département d'Immunologie, Immunopharmacologie, et Pathologie [Equipe de pathologie expérimentale et de neurologie clinique], Illkirch, France.
P F
PF
Kennel
P
P
Poindron
J M
JM
Warter
P
P
Fonteneau
D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced* / Q000503:physiopathology; D002038:Bungarotoxins / Q000008:administration & dosage*; D004195:Disease Models, Animal; D005260:Female; D007114:Immunization; D051379:Mice; D008810:Mice, Inbred C57BL; D009157:Myasthenia Gravis / Q000139:chemically induced* / Q000503:physiopathology; D011950:Receptors, Cholinergic; D009435:Synaptic Transmission / Q000502:physiology
D002038:Bungarotoxins; D011950:Receptors, Cholinergic