Abstract

We examined the involvement of nitric oxide (NO) in ischemic brain damage using hippocampal slices prepared from 30 day old albino rats and exposed to 20 min of oxygen/glucose deprivation (ischemia) followed by 90 min postincubation in oxygen- and glucose-containing media. Damage in the CA1 region was rated on a 0 (intact) to 4 (severe neuronal damage) scale by a rater blind to the experimental condition. Control slices exposed to ischemia were rated as 2.8 ± 0.4 (N = 12); L-N(G)-Monomethylarginine and L-N(G)-nitroarginine (100 μM), non-selective NO synthase (NOS) inhibitors, diminished ischemic damage (0.6 ± 0.3, N = 8, and 1.0 ± 0.5, N = 4, respectively). An inhibitor of brain NOS, 7-nitroindazole (30 μM), was also effective-against ischemic degeneration (0.7 ± 0.3, N = 5). These results suggest that activation of NOS is involved in ischemic degeneration in the CA1 region.

Original languageEnglish
Pages (from-to)157-160
Number of pages4
JournalNeuroscience Letters
Volume210
Issue number3
DOIs
StatePublished - 1996

Keywords

  • 7-Nitroindazole
  • Cerebral ischemia
  • Excitotoxicity
  • Hippocampal slices
  • N-Methyl-D-aspartate
  • Nitric oxide synthase inhibitor

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