Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge

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Standard

Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge. / Lauritzen, M.; Hansen, A. J.; Kronborg, D.; Wieloch, T.

I: Journal of Cerebral Blood Flow and Metabolism, Bind 10, Nr. 1, 01.01.1990, s. 115-122.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Lauritzen, M, Hansen, AJ, Kronborg, D & Wieloch, T 1990, 'Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge', Journal of Cerebral Blood Flow and Metabolism, bind 10, nr. 1, s. 115-122. https://doi.org/10.1038/jcbfm.1990.14

APA

Lauritzen, M., Hansen, A. J., Kronborg, D., & Wieloch, T. (1990). Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge. Journal of Cerebral Blood Flow and Metabolism, 10(1), 115-122. https://doi.org/10.1038/jcbfm.1990.14

Vancouver

Lauritzen M, Hansen AJ, Kronborg D, Wieloch T. Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge. Journal of Cerebral Blood Flow and Metabolism. 1990 jan 1;10(1):115-122. https://doi.org/10.1038/jcbfm.1990.14

Author

Lauritzen, M. ; Hansen, A. J. ; Kronborg, D. ; Wieloch, T. / Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge. I: Journal of Cerebral Blood Flow and Metabolism. 1990 ; Bind 10, Nr. 1. s. 115-122.

Bibtex

@article{e36372268a6e4b40a57cc816f93d3da5,
title = "Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge",
abstract = "The present study aimed to study the relation between the release of arachidonic acid (AA) and the energy state in cerebral cortices of rats during single episodes of cortical spreading depression (CSD). The changes in concentrations of AA, labile phosphate compounds [ATP, ADP, AMP, and phosphocreatine (PCr)], and glycolytic metabolites (lactate, pyruvate, glucose, and glycogen) were studied during and following the large change of the local direct current (DC) potential. Free AA increased markedly during the DC shift, continued to increase during the subsequent 3 min, and returned to control levels at 4-5 min after CSD. PCr decreased by 38% in the first minutes following the DC shift, while ADP increased by 38%. Both returned to normal within a few minutes. ATP, AMP, and energy charge remained constant throughout the experimental period. Glucose decreased by 47% and glycogen by 34% for a few minutes following CSD, while lactate increased by 105% at 2-3 min and by 77% at 4-5 min after CSD. The metabolites returned to control levels at 10 min after CSD. Considering the constant energy charge at all time points during CSD, it is suggested that the AA rise reflects augmented phospholipase activity due to either increased intracellular [Ca2+] or receptor stimulation or both. The possibility that N-methyl-D-aspartate receptors play a role in the release of AA, and that free AA in turn could be part of the mechanism of CSD, is discussed.",
keywords = "arachidonic acid, cortical spreading depression, energy metabolism, extracellular ions",
author = "M. Lauritzen and Hansen, {A. J.} and D. Kronborg and T. Wieloch",
year = "1990",
month = jan,
day = "1",
doi = "10.1038/jcbfm.1990.14",
language = "English",
volume = "10",
pages = "115--122",
journal = "Journal of Cerebral Blood Flow and Metabolism",
issn = "0271-678X",
publisher = "SAGE Publications",
number = "1",

}

RIS

TY - JOUR

T1 - Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge

AU - Lauritzen, M.

AU - Hansen, A. J.

AU - Kronborg, D.

AU - Wieloch, T.

PY - 1990/1/1

Y1 - 1990/1/1

N2 - The present study aimed to study the relation between the release of arachidonic acid (AA) and the energy state in cerebral cortices of rats during single episodes of cortical spreading depression (CSD). The changes in concentrations of AA, labile phosphate compounds [ATP, ADP, AMP, and phosphocreatine (PCr)], and glycolytic metabolites (lactate, pyruvate, glucose, and glycogen) were studied during and following the large change of the local direct current (DC) potential. Free AA increased markedly during the DC shift, continued to increase during the subsequent 3 min, and returned to control levels at 4-5 min after CSD. PCr decreased by 38% in the first minutes following the DC shift, while ADP increased by 38%. Both returned to normal within a few minutes. ATP, AMP, and energy charge remained constant throughout the experimental period. Glucose decreased by 47% and glycogen by 34% for a few minutes following CSD, while lactate increased by 105% at 2-3 min and by 77% at 4-5 min after CSD. The metabolites returned to control levels at 10 min after CSD. Considering the constant energy charge at all time points during CSD, it is suggested that the AA rise reflects augmented phospholipase activity due to either increased intracellular [Ca2+] or receptor stimulation or both. The possibility that N-methyl-D-aspartate receptors play a role in the release of AA, and that free AA in turn could be part of the mechanism of CSD, is discussed.

AB - The present study aimed to study the relation between the release of arachidonic acid (AA) and the energy state in cerebral cortices of rats during single episodes of cortical spreading depression (CSD). The changes in concentrations of AA, labile phosphate compounds [ATP, ADP, AMP, and phosphocreatine (PCr)], and glycolytic metabolites (lactate, pyruvate, glucose, and glycogen) were studied during and following the large change of the local direct current (DC) potential. Free AA increased markedly during the DC shift, continued to increase during the subsequent 3 min, and returned to control levels at 4-5 min after CSD. PCr decreased by 38% in the first minutes following the DC shift, while ADP increased by 38%. Both returned to normal within a few minutes. ATP, AMP, and energy charge remained constant throughout the experimental period. Glucose decreased by 47% and glycogen by 34% for a few minutes following CSD, while lactate increased by 105% at 2-3 min and by 77% at 4-5 min after CSD. The metabolites returned to control levels at 10 min after CSD. Considering the constant energy charge at all time points during CSD, it is suggested that the AA rise reflects augmented phospholipase activity due to either increased intracellular [Ca2+] or receptor stimulation or both. The possibility that N-methyl-D-aspartate receptors play a role in the release of AA, and that free AA in turn could be part of the mechanism of CSD, is discussed.

KW - arachidonic acid

KW - cortical spreading depression

KW - energy metabolism

KW - extracellular ions

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U2 - 10.1038/jcbfm.1990.14

DO - 10.1038/jcbfm.1990.14

M3 - Journal article

C2 - 2105327

AN - SCOPUS:0025069817

VL - 10

SP - 115

EP - 122

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

SN - 0271-678X

IS - 1

ER -

ID: 201456255