Bioenergetic actions of β-bungarotoxin, dendrotoxin and bee-venom phospholipase A2 on guinea-pig synaptosomes

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Abstract
Low concentrations of .beta.-bungarotoxin or bee-venom phospholipase A2 cause a progressive Ca2+-dependent increase in the proton permeability of the mitochondria within the synaptosomal cytosol, manifested as an increase in oligomycin-insensitive respiration and a partial depolarization of the mitochondrial membrane potential. This upcoupling appears to be a consequence of fatty acids liberated by phospholipase A2 activity at the plasma membrane, since it can be mimicked by the addition of oleate-albumin complexes, in which case there is no requirement for external Ca2+. Dendrotoxin does not affect the mitochondrial proton permeability in situ, but protects partially against the uncoupling action of .beta.-bungarotoxin. This effect of bee-venom phospholipase A2 is unaffected by dendrotoxin. .beta.-Bungarotoxin, but not bee-venom phospholipase A2 induces, a slow progressive depolarization of the plasma membrane. The action of .beta.-bungarotoxin at the plasma membrane appears not to be related to fatty acid production, since it is augmented rather than inhibited by raising albumin concentrations in the medium. Apparently, .beta.-bungarotoxin has at least 2 actions on intact synaptosomes, both of which may involve interaction at the plasma membrane with a site common to dendrotoxin: 1st, a mitochondrial uncoupling mediated by fatty acids and, secondly, a depolarization at the plasma membrane.

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