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

Lauritzen, M. ; Hansen, A. J. ; Kronborg, D. and Wieloch, T. LU (1990) In Journal of Cerebral Blood Flow and Metabolism 10(1). p.115-122
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... (More)

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.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
arachidonic acid, cortical spreading depression, energy metabolism, extracellular ions
in
Journal of Cerebral Blood Flow and Metabolism
volume
10
issue
1
pages
115 - 122
publisher
Nature Publishing Group
external identifiers
  • scopus:0025069817
  • pmid:2105327
ISSN
0271-678X
DOI
10.1038/jcbfm.1990.14
language
English
LU publication?
yes
id
34d34d19-306a-4056-9b53-c3b35114a868
date added to LUP
2019-06-13 17:38:00
date last changed
2024-01-01 10:30:36
@article{34d34d19-306a-4056-9b53-c3b35114a868,
  abstract     = {{<p>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 [Ca<sup>2+</sup>] 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.</p>}},
  author       = {{Lauritzen, M. and Hansen, A. J. and Kronborg, D. and Wieloch, T.}},
  issn         = {{0271-678X}},
  keywords     = {{arachidonic acid; cortical spreading depression; energy metabolism; extracellular ions}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{115--122}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Journal of Cerebral Blood Flow and Metabolism}},
  title        = {{Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge}},
  url          = {{http://dx.doi.org/10.1038/jcbfm.1990.14}},
  doi          = {{10.1038/jcbfm.1990.14}},
  volume       = {{10}},
  year         = {{1990}},
}