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Inciting excitotoxic cytocide among central neurons
Advances in Experimental Medicine and Biology
|January 1, 1986
Summary
Epilepsy and anoxia cause brain damage similar to that from glutamate (Glu). Drugs blocking Glu excitotoxicity, like ketamine, protect against this seizure-related damage, suggesting a common mechanism.
Area of Science:
- Neuroscience
- Pathology
- Pharmacology
Background:
- Sustained limbic seizures are linked to acute brain damage.
- This damage resembles excitotoxicity induced by glutamate (Glu).
Purpose of the Study:
- To review evidence linking seizure-related brain damage to excitotoxicity.
- To explore the role of glutamate receptors in seizure and anoxic brain damage.
- To investigate the protective effects of NMDA receptor antagonists.
Main Methods:
- Review of electron microscopic studies on seizure-induced brain damage.
- Analysis of studies on persistent axonal tract stimulation and neuronal degeneration.
- Examination of the effects of phencyclidine and ketamine on seizure-related brain damage.
Main Results:
- Seizure-induced brain damage is ultrastructurally similar to excitotoxic damage.
- Stimulation of Glu-releasing tracts causes excitotoxic degeneration.
- Phencyclidine and ketamine protect against seizure-related brain damage, suggesting anticonvulsant or antiexcitotoxic effects.
- Excitotoxicity may underlie both seizure-mediated and anoxic brain damage.
Conclusions:
- Glutamate excitotoxicity is a key mechanism in seizure-related brain damage.
- Understanding excitotoxic mechanisms could lead to new treatments for epilepsy and anoxia-induced brain injury.