Abstract
The ability of diphenylhydantoin (DPH) to prevent hypoxia-induced [3H]glutamate release was examined in perfused rat hippocampal slices. Hypoxia (25 min; 95% N2/5% CO2) caused a prolonged release of [3H]glutamate, which was reduced significantly if DPH (20 μM) was present from the beginning of the perfusion. Perfusion with oxygenated medium (reoxygenation) following hypoxia also caused a pronounced release of glutamate. A therapeutic concentration of DPH, added before, during, or after hypoxia, decreased this release of glutamate. These results suggest that DPH may protect against glutamate-mediated neurotoxicity associated with stroke.
Original language | English (US) |
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Pages (from-to) | 127-130 |
Number of pages | 4 |
Journal | Brain research |
Volume | 558 |
Issue number | 1 |
DOIs | |
State | Published - Aug 30 1991 |
Keywords
- Diphenylhydantoin
- Glutamate
- Hippocampus
- Hypoxia
- Ischemia
- Phenytoin
- Stroke
ASJC Scopus subject areas
- Clinical Neurology
- Molecular Biology
- General Neuroscience
- Developmental Biology