Phenytoin protects against hypoxia-induced death of cultured hippocampal neurons

F. H. Boehm, L. K. Liem, P. K. Stanton, P. E. Potter, J. R. Moskal*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


The neuroprotective actions of the anticonvulsant phenytoin (diphenylhydantoin, PHT) were evaluated using 3 week old primary hippocampal cultures derived from 19 day embryonic rat. When added to the culture medium prior to a hypoxic insult, PHT increased neuronal viability two-fold. Doubling extracellular Mg2+ concentration was similarly neuropotective. In contrast, PHT was unable to protect against hypoxia-induced death in one week old cultures, nor was PHT protective against N-methyl-d-aspartate (NMDA)-induced neurotoxicity in cultures of either age. These findings suggest that non-NMDA receptor mechanisms are important in hypoxia-induced neuronal death, and may have important implications for the treatment of stroke.

Original languageEnglish (US)
Pages (from-to)171-174
Number of pages4
JournalNeuroscience Letters
Issue number1-2
StatePublished - Jul 4 1994


  • CA1
  • Delayed cell death
  • Diphenylhydantoin
  • Hippocampus
  • Ischemia
  • NMDA receptor
  • Phenytoin
  • Primary hippocampal culture
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)


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