On the blockade of acetylcholine release at mouse motor nerve terminals by β-bungarotoxin and crotoxin

β-Bungarotoxin and crotoxin are phospholipase A₂ neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preperations. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by β-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K⁺-induced depolarization and by the Ca²⁺-ionophore A23187. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.