Capsaicin-sensitive mechanisms are involved in cortical spreading depression-associated cerebral blood flow changes in rats

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Abstract

We tested the hypothesis that capsaicin-sensitive mechanisms play a role in the cortical spreading depression (CSD)-related changes in cortical blood flow (CBF). CBF was measured with laser Doppler flowmetry in anesthetized rats. The animals were treated with capsaicin before (48 h-2 weeks) or during the experiments. This agent is thought to stimulate small-diameter sensory nerve fibers selectively and to deplete stored peptides. In the vehicle-treated group (n = 8), the peak value of the CSD-associated hyperperfusion was 257 ± 12% above the baseline (mean ± SEM, P <0.05). In the groups treated with 20 and 40 μg/kg or 20 mg/kg capsaicin, there were only small decreases in CBF. In the groups treated with 100 mg/kg capsaicin, the CSD-associated hyperemia was reduced at 48 h (158 ± 7%, P <0.05). However, at 96 h a transient hyperresponsiveness (390 ± 38%, P <0.05) was observed, which had disappeared by 2 weeks. These results indicate that the manipulation of sensory neuropeptide stores results in a biphasic effect on CSD-induced CBF responses. (C) 2000 Elsevier Science Ireland Ltd.

Original languageEnglish
Pages (from-to)17-20
Number of pages4
JournalNeuroscience Letters
Volume292
Issue number1
DOIs
Publication statusPublished - Sep 29 2000

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Cerebrovascular Circulation
Cortical Spreading Depression
Capsaicin
Laser-Doppler Flowmetry
Hyperemia
Neuropeptides
Nerve Fibers
Peptides

Keywords

  • Capsaicin
  • Cortical spreading depression
  • Laser Doppler
  • Rat
  • Trigeminal nerve

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Capsaicin-sensitive mechanisms are involved in cortical spreading depression-associated cerebral blood flow changes in rats",
abstract = "We tested the hypothesis that capsaicin-sensitive mechanisms play a role in the cortical spreading depression (CSD)-related changes in cortical blood flow (CBF). CBF was measured with laser Doppler flowmetry in anesthetized rats. The animals were treated with capsaicin before (48 h-2 weeks) or during the experiments. This agent is thought to stimulate small-diameter sensory nerve fibers selectively and to deplete stored peptides. In the vehicle-treated group (n = 8), the peak value of the CSD-associated hyperperfusion was 257 ± 12{\%} above the baseline (mean ± SEM, P <0.05). In the groups treated with 20 and 40 μg/kg or 20 mg/kg capsaicin, there were only small decreases in CBF. In the groups treated with 100 mg/kg capsaicin, the CSD-associated hyperemia was reduced at 48 h (158 ± 7{\%}, P <0.05). However, at 96 h a transient hyperresponsiveness (390 ± 38{\%}, P <0.05) was observed, which had disappeared by 2 weeks. These results indicate that the manipulation of sensory neuropeptide stores results in a biphasic effect on CSD-induced CBF responses. (C) 2000 Elsevier Science Ireland Ltd.",
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