Neuroprotective effects of anticonvulsants in rat hippocampal slice cultures exposed to oxygen/glucose deprivation

Research output: Contribution to journalJournal articleResearchpeer-review

Some anticonvulsants show neuroprotective effects, and may be of use in reducing neuronal death resulting from stroke or traumatic brain injury. Here I report that a broad range of anticonvulsants protect cells in hippocampal slice cultures from death induced by oxygen/glucose deprivation (OGD). Hippocampal slice cultures were submitted to 1 h OGD and the resulting cell death was quantified 24 h later using a novel automated fluorescent scanning method. The classical anticonvulsants phenobarbital, phenytoin, ethosuximide, chlordiazepoxide and midazolam all significantly and dose-dependently reduced cell death induced by OGD. The newer anticonvulsants carbamazepine, felbamate, lamotrigine, tiagabine, and oxcarbazepine also had significant neuroprotective effects, but gabapentin, valproic acid (10 mM), levetiracetam and retigabine were not neuroprotective at a concentration up to 300 microM. In conclusion, several classical and newer anticonvulsants have neuroprotective properties in an in vitro model that simulates cerebral ischemia.
Original languageEnglish
JournalNeuroscience Letters
Volume335
Issue number3
Pages (from-to)167-70
Number of pages3
ISSN0304-3940
Publication statusPublished - 2003

Bibliographical note

Keywords: Acetic Acids; Amines; Animals; Anoxia; Anticonvulsants; Carbamates; Carbamazepine; Cell Death; Cells, Cultured; Chlordiazepoxide; Cyclohexanecarboxylic Acids; Dose-Response Relationship, Drug; Ethosuximide; Glucose; Hippocampus; Ischemia; Midazolam; Neurons; Neuroprotective Agents; Nipecotic Acids; Phenobarbital; Phenylcarbamates; Phenylenediamines; Phenytoin; Piracetam; Propylene Glycols; Rats; Rats, Wistar; Triazines; Valproic Acid; gamma-Aminobutyric Acid

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