Differential roles of cyclooxygenase isoforms after kainic acid-induced prostaglandin E 2 production and neurodegeneration in cortical and hippocampal cell cultures

Eun Joo Kim, Jongeun Lee, Kyung Ja Kwon, Soo Hwan Lee, Chang Hyun Moon, Eun Joo Baik

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Prostaglandins, which are cyclooxygenase (COX) products, are pathologically up-regulated, and have been proven to be closely associated with neuronal death. In this study, we investigated a role of COX isoforms (COX-1 and COX-2) in kainic acid-induced neuronal death in cultured murine cortical or hippocampal neurons. In primary cortical neurons, both indomethacin (COX-1/-2 nonselective inhibitor) and aspirin (COX-1 preferential inhibitor) reduced basal and kainic acid-induced PGE 2 production significantly and prevented neuronal cell death after kainic acid treatment. In contrast, NS398 (COX-2 selective inhibitor) had no effect on kainic acid-induced neuronal cell death. In hippocampal neurons, however, COX-2 inhibitors prevented both kainic acid-induced neuronal death and PGE 2 production. COX-2 expression was remarkably up-regulated by kainic acid in hippocampal neurons; whereas in cortical neurons, COX-2 expression was comparatively less significant. Astrocytes were unresponsive to kainic acid in terms of PGE 2 production and cell death. In conclusion, we suggest that the release of PGE 2 induced by kainic acid occurred through COX-1 activity rather than COX-2 in cortical neurons. The inhibition of PGE 2 release by COX-1 inhibitors prevented kainic acid-induced cortical neuronal death, while in the hippocampal neurons, COX-2 inhibitors prevented kainic acid-induced PGE 2 release and hippocampal neuronal death.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalBrain Research
Issue number1
Publication statusPublished - 2001 Jul 10


All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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