Neurochemical Research

, Volume 8, Issue 2, pp 159–166 | Cite as

Failure of atractyloside to inhibit synaptosomal mitochondrial energy transduction

  • M. Anthony Verity
  • W. Jann Brown
  • M. K. Cheung
Original Articles


Studies on synaptosome mitochondrial respiration are complicated by “free” mitochondria. Veratridine stimulation of synaptosomal respiration was due to increased Na+ cycling at the synaptosome membrane associated with increased oxidative phosphorylation of intraterminal ADP and was inhibited by oligomycin, ouabain or Na+ free medium. Atractylate or carboxyatractyloside failed to block veratridine-stimulated respiration but inhibited exogenous-ADP-stimulated respiration. Protein synthesis in the synaptosome fraction was inhibited by oligomycin, valinomycin or 2,4-dinitrophenol but was unaffected by excess atractylate. No change in synaptosomal adenine nucleotide content was found in the presence of atractylate, although a significant decrease in the [ATP]/[ADP] was found with oligomycin, veratridine or valinomycin. These findings show that atractylate does not modify intraterminal mitochondrial energy transduction and indirectly suggest an impermeability of the synaptosome membrane to atractylate.


Nucleotide Protein Synthesis Adenine Oxidative Phosphorylation Ouabain 
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Copyright information

© Plenum Publishing Corporation 1983

Authors and Affiliations

  • M. Anthony Verity
    • 1
    • 2
  • W. Jann Brown
    • 1
    • 2
  • M. K. Cheung
    • 1
    • 2
  1. 1.Department of Pathology (Neuropathology)Brain Research InstituteLos Angeles
  2. 2.Mental Retardation Research CenterUCLA Center for the Health SciencesLos Angeles

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