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  • 标题:Uptake of 1-Methyl-4-phenylpyridinium Ion (MPP+) and ATP Content in Synaptosomes
  • 本地全文:下载
  • 作者:Masami MATSUNAGA ; Yoshihiro SHIRANE ; Toshihiro AIUCHI
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:1996
  • 卷号:19
  • 期号:1
  • 页码:29-33
  • DOI:10.1248/bpb.19.29
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要:Symptoms such as those in Parkinson's disease are known to be induced by the neurotoxin, 1-methyl-4-phenylpyridinium (MPP+). We tried to quantitatively measure synaptosomal MPP+ uptake using an MPP+ selective electrode to study the correlation between MPP+ uptake and respiratory inhibition. Synaptosomal MPP+ uptake was low but could be increased by the addition of glucose as an energy substrate, or increased with an increase in the concentration of MPP+. The rate of uptake was 0.2 nmol/mg protein/min at 50μM MPP+. Tetraphenylboron (TPB-), which enhances cation permeability, increased MPP+ uptake, and the increase was proportional to the TPB- concention. When external MPP+ concentration was increased above 200μM, ATP was depleted and the uptake of MPP+ decreased, which resulted in the release of intrasynaptosomal MPP+. MPP+ uptake was also decreased by depolarization of the membrane potential in synaptosomes. MPP+ was presumed to be distributed across both the synaptosomal and inner mitochondrial membranes, and to be affected by membrane potential as a lipophilic cation. When respiration of the inner mitochondria was inhibited by increasing the intrasynaptosomal MPP+ concentration, the concentration of MPP+ in cytosol was presumed to increase by the release of MPP+ from the mitochondria, and synaptosomal MPP+ uptake would then be decreased.
  • 关键词:1-methyl-4-phenylpyridinium ion;tetraphenylboron;synaptosome
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