Kainic acid rapidly induces cyclooxygenase (COX)-2 in piglet cerebral cortex

Ferenc Domoki, Nishadi Thrikawala, Gregory S. Robins, Ferenc Bari, David W. Busija

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6 Citations (Scopus)

Abstract

Ischemia/reperfusion (I/R) results in a robust induction of cyclooxygenase (COX)-2 in the newborn brain via unknown mechanisms, but glutamate release and activation of KA receptors may be involved. We examined effects of local KA (3-300 μmol/l for 10 min) treatment on cortical COX-2 expression in anesthetized piglets using a closed cranial window. Treated and corresponding control tissue samples were collected 0.5-10 h after treatment. COX-2 mRNA and protein levels were assessed using RNase protection assay and immunohistochemistry, respectively. KA elicited reproducible dose-dependent increases in cortical COX-2 mRNA unaffected by indomethacin or N(G)-nitro-L-arginine methyl ester pretreatment. COX-2 mRNA levels were elevated at 30 min, peaked at 2 h, but remained enhanced for up to 10 h after KA. Neuronal COX-2 immunoreactivity was also enhanced compared with the control side in all cortical layers 8 h after KA. In summary, activation of KA receptors may be involved in the neuronal induction of COX-2 after I/R in the newborn. (C) 2000 Lippincott Williams and Wilkins.

Original languageEnglish
Pages (from-to)3435-3438
Number of pages4
JournalNeuroreport
Volume11
Issue number16
DOIs
Publication statusPublished - Nov 9 2000

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Keywords

  • Indomethacin
  • Prostaglandin H-synthase
  • Ribonuclease protection assay
  • mRNA

ASJC Scopus subject areas

  • Neuroscience(all)

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