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Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission.

  • Author(s): Hennebelle, Marie
  • Zhang, Zhichao
  • Metherel, Adam H
  • Kitson, Alex P
  • Otoki, Yurika
  • Richardson, Christine E
  • Yang, Jun
  • Lee, Kin Sing Stephen
  • Hammock, Bruce D
  • Zhang, Liang
  • Bazinet, Richard P
  • Taha, Ameer Y
  • et al.
Abstract

Linoleic acid (LA; 18:2 n-6), the most abundant polyunsaturated fatty acid in the US diet, is a precursor to oxidized metabolites that have unknown roles in the brain. Here, we show that oxidized LA-derived metabolites accumulate in several rat brain regions during CO2-induced ischemia and that LA-derived 13-hydroxyoctadecadienoic acid, but not LA, increase somatic paired-pulse facilitation in rat hippocampus by 80%, suggesting bioactivity. This study provides new evidence that LA participates in the response to ischemia-induced brain injury through oxidized metabolites that regulate neurotransmission. Targeting this pathway may be therapeutically relevant for ischemia-related conditions such as stroke.

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