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Enhanced hippocampal F 2 ‐isoprostane formation following kainate‐induced seizures
Author(s) -
Patel Manisha,
Liang LiPing,
Roberts II L. Jackson
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00659.x
Subject(s) - kainate receptor , hippocampal formation , chemistry , kainic acid , dentate gyrus , lipid peroxidation , status epilepticus , endocrinology , medicine , oxidative stress , epilepsy , biochemistry , biology , glutamate receptor , neuroscience , ampa receptor , receptor
We attempted to obtain evidence for the occurrence of oxidant injury following seizure activity by measuring hippocampal F 2 ‐isoprostanes ( F 2 ‐IsoPs), a reliable marker of free radical‐induced lipid peroxidation. Formation of F 2‐ IsoPs esterified in hippocampal phospholipids was correlated with hippocampal neuronal loss and mitochondrial aconitase inactivation, a marker of superoxide production in the kainate model. F 2 ‐IsoPs were measured in microdissected hippocampal CA1, CA3 and dentate gyrus (DG) regions at various times following kainate administration. Kainate produced a large increase in F 2 ‐IsoP levels in the highly vulnerable CA3 region 16 h post injection. The CA1 region showed small, but statistically insignificant increases in F 2 ‐IsoP levels. Interestingly, the DG, a region resistant to kainate‐induced neuronal death also showed marked (2.5–5‐fold) increases in F 2 ‐IsoP levels 8, 16, and 24 h post injection. The increases in F 2 ‐Isop levels in CA3 and DG were accompanied by inactivation of mitochondrial aconitase in these regions. This marked subregion‐specific increase in F 2 ‐Isop following kainate administration suggests that oxidative lipid damage results from seizure activity and may play an important role in seizure‐induced death of vulnerable neurons.