Metabolism of oleoyl-CoA in rat brain synaptosomes: effects of calcium and post-decapitative ischemia.

The hydrolysis of acyl-CoA by acyl-CoA hydrolase (EC 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.
AuthorsJ Strosznajder, W Tang, R Manning, A Y Lin, R MacQuarrie, G Y Sun
JournalNeurochemical research (Neurochem Res) Vol. 6 Issue 11 Pg. 1231-40 (Nov 1981) ISSN: 0364-3190 [Print] UNITED STATES
PMID6123958 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Acyl Coenzyme A
  • oleoyl-coenzyme A
  • Palmitoyl-CoA Hydrolase
  • Calcium
  • Acyl Coenzyme A (metabolism)
  • Animals
  • Brain Ischemia (metabolism)
  • Calcium (pharmacology)
  • Cerebral Cortex (blood supply, metabolism)
  • Intracellular Membranes (enzymology)
  • Palmitoyl-CoA Hydrolase (antagonists & inhibitors)
  • Rats
  • Rats, Inbred Strains
  • Synaptosomes (drug effects, metabolism)

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