Diphenylhydantoin protects against hypoxia-induced impairment of hippocampal synaptic transmission

Patric K. Stanton*, Joseph R. Moskal

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


The ability of diphenylhydantoin (DPH) to protect against hypoxia-induced neuronal damage was examined using electrophysiological recordings of extracellular evoked potentials from CA1 pyramidal neurons of rat hippocampal slices in vitro. In normal medium, a 15-min hypoxic insult (95% N2/5% CO2) produced rapid and complete loss of Schaffer collateral synaptic transmission, which only recovered to 20% of pre-hypoxia values after 90 min of reoxygenation. DPH (20 μM) bath applied prior to onset of hypoxia slowed the loss of transmission during hypoxia, and led to 75% recovery of evoked potentials upon reoxygenation. Thus, DPH appears to protect against hypoxia-induced loss of synaptic transmission, and may thereby lessen neuronal damage and cognitive dysfunction associated with stroke.

Original languageEnglish (US)
Pages (from-to)351-354
Number of pages4
JournalBrain research
Issue number2
StatePublished - Apr 19 1991


  • CA1
  • Calcium
  • Diphenylhydantoin
  • Hippocampus
  • Hypoxia
  • Ischemia
  • Phenytoin
  • Plasticity
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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