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

Marie Hennebelle, Zhichao Zhang, Adam H. Metherel, Alex P. Kitson, Yurika Otoki, Christine E. Richardson, Jun Yang, Kin Sing Stephen Lee, Bruce D. Hammock, Liang Zhang, Richard P. Bazinet, Ameer Y. Taha

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish (US)
Article number4342
JournalScientific Reports
Volume7
Issue number1
DOIs
StatePublished - Dec 1 2017

Fingerprint

Linoleic Acid
Synaptic Transmission
Brain Injuries
Ischemia
Brain
Unsaturated Fatty Acids
Hippocampus
Stroke
Diet

ASJC Scopus subject areas

  • General

Cite this

Hennebelle, M., Zhang, Z., Metherel, A. H., Kitson, A. P., Otoki, Y., Richardson, C. E., ... Taha, A. Y. (2017). Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission. Scientific Reports, 7(1), [4342]. https://doi.org/10.1038/s41598-017-02914-7

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

In: Scientific Reports, Vol. 7, No. 1, 4342, 01.12.2017.

Research output: Contribution to journalArticle

Hennebelle, M, Zhang, Z, Metherel, AH, Kitson, AP, Otoki, Y, Richardson, CE, Yang, J, Lee, KSS, Hammock, BD, Zhang, L, Bazinet, RP & Taha, AY 2017, 'Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission', Scientific Reports, vol. 7, no. 1, 4342. https://doi.org/10.1038/s41598-017-02914-7
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. / Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission. In: Scientific Reports. 2017 ; Vol. 7, No. 1.
@article{6e0476ab0c6f47a4b1c02ca031cf0e1e,
title = "Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission",
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.",
author = "Marie Hennebelle and Zhichao Zhang and Metherel, {Adam H.} and Kitson, {Alex P.} and Yurika Otoki and Richardson, {Christine E.} and Jun Yang and Lee, {Kin Sing Stephen} and Hammock, {Bruce D.} and Liang Zhang and Bazinet, {Richard P.} and Taha, {Ameer Y.}",
year = "2017",
month = "12",
day = "1",
doi = "10.1038/s41598-017-02914-7",
language = "English (US)",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission

AU - Hennebelle, Marie

AU - Zhang, Zhichao

AU - Metherel, Adam H.

AU - Kitson, Alex P.

AU - Otoki, Yurika

AU - Richardson, Christine E.

AU - Yang, Jun

AU - Lee, Kin Sing Stephen

AU - Hammock, Bruce D.

AU - Zhang, Liang

AU - Bazinet, Richard P.

AU - Taha, Ameer Y.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85021634988&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85021634988&partnerID=8YFLogxK

U2 - 10.1038/s41598-017-02914-7

DO - 10.1038/s41598-017-02914-7

M3 - Article

AN - SCOPUS:85021634988

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 4342

ER -