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Metabolism of oleoyl-CoA in rat brain synaptosomes

Effects of calcium and post-decapitative ischemia

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Abstract

The hydrolysis of acyl-CoA by acyl-CoA hydrolase (EC 3.1.2.2.) in brain synaptosomes was inhibited by calcium. This inhibition was partly due to interaction of Ca2+ with the acyl-CoA, which was present in the soluble form, and partly due to complex formation among acyl-CoA, Ca2+ and membrane phospholipids. The inhibition of acyl-CoA hydrolase activity, as well as the complex formation. could be reversed if incubation was carried out in the presence of Ca2+ chelating agents. Synaptosomes isolated from brain samples after 1 min of postdecapitative treatment showed a decrease in oleoyl-CoA hydrolase activity. The physiological implication of acyl-CoA metabolism in relation to synaptic function is discussed.

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Abbreviations

FFA:

Free fatty acids

GPC:

glycerophosphocholines

GPE:

glycerophosphoethanolamines

GPI:

glycerophosphoinositols

GPS:

glycerophosphoserines

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Authors and Affiliations

  1. Department of Neurochemistry Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

    J. Strosznajder

  2. Sinclair Comparative Medicine Research Farm and Biochemistry Department, University of Missouri, Columbia, Missouri

    W. Tang, R. Manning & G. Y. Sun

  3. Chemistry Department, University of Missouri, Kansas City, Missouri

    A. Y-T. Lin & R. MacQuarrie

Authors
  1. J. Strosznajder
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  2. W. Tang
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  3. R. Manning
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  4. A. Y-T. Lin
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  5. R. MacQuarrie
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  6. G. Y. Sun
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Strosznajder, J., Tang, W., Manning, R. et al. Metabolism of oleoyl-CoA in rat brain synaptosomes. Neurochem Res 6, 1231–1240 (1981). https://doi.org/10.1007/BF00966680

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  • DOI: https://doi.org/10.1007/BF00966680

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