Ultrastructure of botulinum type-A poisoned frog motor nerve terminals after enhanced quantal transmitter release caused by carbonyl cyanide m-chlorophenylhydrazone.
The effects of carbonyl cyanide m-chlorophenylhydrazone (CCCP) on spontaneous quantal transmitter release and nerve terminal ultrastructure were studied on isolated cutaneous pectoris nerve-muscle preparations from frogs that were completely paralysed by a single sublethal dose of Clostridium botulinum type A toxin (BoTx). CCCP enhanced miniature endplate potential frequency at poisoned junctions and caused a reduction in the density of clear synaptic vesicles and of large dense core vesicles in motor nerve terminals. However, the intensity of these effects was much less important than that previously reported at unpoisoned junctions. The moderate depletion of synaptic vesicles can be related to the low levels of transmitter release detected with CCCP at BoTx-poisoned terminals.
Pécot-Dechavassine
M
M
Département de Cytologie, Institut des Neurosciences du CNRS, Université Pierre et Marie Curie, Paris, France.
Molgo
J
J
Thesleff
S
S
D000818:Animals; D001905:Botulinum Toxins / Q000633:toxicity*; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology*; D066298:In Vitro Techniques; D009045:Motor Endplate / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure*; D009132:Muscles / Q000294:innervation; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011896:Rana temporaria
D018377:Neurotransmitter Agents; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D001905:Botulinum Toxins