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

Authors
Kim, EJ; Lee, JE; Kwon, KJ; Lee, SH; Moon, CH; Baik, EJ
Citation
Brain research, 908(1):1-9, 2001
Journal Title
Brain research
ISSN
0006-89931872-6240
Abstract
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.
MeSH terms
AnimalsAstrocytes/cytologyAstrocytes/drug effectsAstrocytes/enzymologyBisbenzimidazole/pharmacokineticsCells, Cultured/cytologyCells, Cultured/enzymologyCerebral Cortex/drug effectsCerebral Cortex/enzymology*Cerebral Cortex/pathologyColoring Agents/pharmacokineticsCyclooxygenase Inhibitors/pharmacologyDinoprostone/metabolism*Dinoprostone/secretionExcitatory Amino Acid Agonists/pharmacologyFetusFluorescent Dyes/pharmacologyGene Expression Regulation, Enzymologic/drug effectsGene Expression Regulation, Enzymologic/physiologyHippocampus/drug effectsHippocampus/enzymology*Hippocampus/pathologyKainic Acid/pharmacologyL-Lactate Dehydrogenase/drug effectsL-Lactate Dehydrogenase/metabolismL-Lactate Dehydrogenase/secretionMiceNerve Degeneration/chemically inducedNerve Degeneration/enzymology*Nerve Degeneration/physiopathologyNeurons/cytologyNeurons/drug effectsNeurons/enzymology*Propidium/pharmacokineticsProstaglandin-Endoperoxide Synthases/drug effectsProstaglandin-Endoperoxide Synthases/metabolism*Protein Isoforms/drug effectsProtein Isoforms/metabolism
PMID
11457426
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
김, 은주이, 수환문, 창현백, 은주
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