Stanton P K, Moskal J R
Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461.
Brain Res. 1991 Apr 19;546(2):351-4. doi: 10.1016/0006-8993(91)91501-q.
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 microM) 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.
