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Oxidative damage in the guinea pig hippocampal slice
1Physiology Department, Armed Forces Radiobiology Research Institute, Bethesda, MD 20814.
Free Radical Biology & Medicine
|January 1, 1989
Summary
Oxidative stress from free radicals contributes to brain damage after ischemia and trauma. This study shows oxidants damage synaptic function but not postsynaptic responses in guinea pig hippocampus.
Area of Science:
- Neuroscience
- Neurophysiology
- Oxidative Stress Research
Background:
- Free radicals and active oxygen species are implicated in brain ischemia and head trauma.
- Previous research indicates free radicals cause synaptic and postsynaptic damage in hippocampal slices.
Purpose of the Study:
- To investigate the role of oxidation in free radical-induced damage.
- To evaluate the effects of specific oxidants on hippocampal electrophysiology.
Main Methods:
- Electrophysiological recordings were performed on hippocampal slices from guinea pigs.
- Neurons in the CA1 region were stimulated to evoke population postsynaptic potentials (PSPs) and population spikes.
- The effects of chloramine-T and N-chlorosuccinimide (NCS) on these responses were analyzed.
Main Results:
- Both chloramine-T and NCS dose-dependently reduced the population spike.
- Population PSPs were significantly decreased by both oxidants.
- The ability of population PSPs to generate population spikes remained unimpaired.
Conclusions:
- Oxidation reactions contribute to synaptic damage observed after free radical exposure.
- Oxidative mechanisms do not fully explain the postsynaptic damage associated with free radicals.