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

Marie HennebelleZhichao ZhangAdam H MetherelAlex P KitsonYurika OtokiChristine E RichardsonJun YangKin Sing Stephen LeeBruce D HammockLiang ZhangRichard P BazinetAmeer Y Taha
Published in: Scientific reports (2017)
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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