Article thumbnail
Location of Repository

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

By D Nicholls, R Snelling and O Dolly

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 uncoupling 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. In contrast, 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. It is concluded that beta-bungarotoxin has at least two actions on intact synaptosomes, both of which may involve interaction at the plasma membrane with a site common to dendrotoxin: first, a mitochondrial uncoupling mediated by fatty acids and, secondly, a depolarization at the plasma membrane

Topics: Research Article
Year: 1985
OAI identifier: oai:pubmedcentral.nih.gov:1145107
Provided by: PubMed Central
Sorry, our data provider has not provided any external links therefore we are unable to provide a link to the full text.

Suggested articles


To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.