Ineffectiveness of 3,4-diaminopyridine as a therapy for type C botulism.
Clostridium botulinum neurotoxins inhibit acetylcholine release at neuromuscular junctions. Agents stimulating neurotransmitter efflux, such as 3,4-diaminopyridine (3,4-DAP), could be useful for botulism therapy. Treatment with 3,4-DAP (8 mg/kg hourly, beginning 3 hr after toxin injection) failed to increase the survival times of mice receiving 10, 20 or 40 LD50 type C, but did prolong the survival of those receiving 20 LD50 type A. This difference in 3,4-DAP efficacy may reflect variations in the molecular mechanism of action of types A and C botulinum neurotoxins.
Pathology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21701.
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Siegel
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Price
D015761:4-Aminopyridine / Q000031:analogs & derivatives*; D000109:Acetylcholine / Q000378:metabolism; D000077770:Amifampridine; D000631:Aminopyridines / Q000627:therapeutic use*; D000818:Animals; D001906:Botulism / Q000188:drug therapy*; D051379:Mice; D009469:Neuromuscular Junction / Q000187:drug effects / Q000378:metabolism
D000631:Aminopyridines; D015761:4-Aminopyridine; D000109:Acetylcholine; D000077770:Amifampridine