Abstract
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 language | English (US) |
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Pages (from-to) | 351-354 |
Number of pages | 4 |
Journal | Brain research |
Volume | 546 |
Issue number | 2 |
DOIs | |
State | Published - Apr 19 1991 |
Funding
This work was supported by the Esther A. and Joseph Klingen-stein Fund (P.K.S.) and by the Health Foundation (J.R.M.).
Keywords
- CA1
- Calcium
- Diphenylhydantoin
- Hippocampus
- Hypoxia
- Ischemia
- Phenytoin
- Plasticity
- Stroke
ASJC Scopus subject areas
- Clinical Neurology
- Molecular Biology
- General Neuroscience
- Developmental Biology