期刊
NEUROSCIENCE RESEARCH
卷 56, 期 1, 页码 103-110出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neures.2006.06.003
关键词
prostaglandin E-2; COX-2; hippocampal neuron death; CA3 region; seizure; kainic acid; selective COX-2 inhibitor; COX-2 knockout mouse
Injection of kainic acid (KA) into the brain causes severe seizures with hippocampal neuron loss. KA has been shown to immediately induce cyclooxygenase-2 (COX-2) expression in hippocampal neurons, indicating that neuronal COX-2 might be involved in neuronal death. In this study, however, we reveal that the delayed COX-2 induction in non-neuronal cells after KA injection plays an important role in hippocampal neuron loss rather than early COX-2 expression in neurons. We find that KA microinjection into the hemilateral hippocampus shows a later induction of COX-2 expression in non-neuronal cells, such as endothelial cells and astrocytes. In the KA-injected side, PGE(2) concentration gradually increases and peaks at 24 h after injection, when non-neuronal COX-2 expression also peaks. When this delayed PGE2 elevation is prevented by selective COX-2 inhibitor NS398, it can block hippocampal cell death. Moreover, COX-2 knockout mice are also resistant to neuronal death after KA treatment. These findings indicate that delayed PGE(2) production by non-neuronal COX-2 may facilitate neuronal death after seizure. Inhibition of COX-2 to an extent similar to PGE(2) elevation after onset of seizure may be useful to prevent neuronal death. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
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