title: The action of batulinum toxin at the neuromuscular junction.
abstract: Botulism results from the action of a protein neurotoxin (mol. wt. congruent to 150,000) produced by the bacterium Clostridium botulinum, of which there are eight known strains. Botulinum neurotoxin is the most potent biological toxin known, having a median lethal dose of 5--50 ng/kg body weight. The primary site of action of botulinum toxin is the cholinergic nerve terminal, where it blocks the release of the neurotransmitter acetylcholine. Death usually results from respiratory failure. Nonlethal doses of botulinum toxin can induce sprouting of the nerve terminal and have significant postsynaptic effects, including muscle atrophy and alterations in the membrane electrical properties of the muscle fiber. There is no universally available treatment for botulinum intoxication. However, immunotherapeutic and chemotherapeutic procedures are not being developed and will be discussed.
mesh_terms: D015761:4-Aminopyridine; D000109:Acetylcholine / Q000037:antagonists & inhibitors; D000077770:Amifampridine; D000631:Aminopyridines / Q000627:therapeutic use; D001905:Botulinum Toxins / Q000494:pharmacology*; D001906:Botulism / Q000276:immunology / Q000628:therapy*; D002118:Calcium / Q000502:physiology; D003014:Clostridium botulinum / Q000472:pathogenicity; D006801:Humans; D009469:Neuromuscular Junction / Q000187:drug effects*; D018377:Neurotransmitter Agents / Q000037:antagonists & inhibitors; D009435:Synaptic Transmission / Q000187:drug effects
chemical_list: D000631:Aminopyridines; D018377:Neurotransmitter Agents; D015761:4-Aminopyridine; D001905:Botulinum Toxins; D000109:Acetylcholine; D000077770:Amifampridine; D002118:Calcium