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Updated: Aug 19, 2026

Electrophoretic Delivery of γ-aminobutyric Acid (GABA) into Epileptic Focus Prevents Seizures in Mice
Published on: May 16, 2019
[Neuroprotective activity of antiepileptic drugs]
Katarzyna Czuczwar1, Mirosław Czuczwar, Jacek Cieszczyk
1Katedra i Zakład Patofizjologii, Akademia Medyczna im. F. Skubiszewskiego, Lublin. czuczwarsj@yahoo.com
Abstract:
Clinical and experimental data indicate that epilepsy may lead to neuronal death and lesions placed in diverse brain regions. Also, the anticonvulsant activity of some antiepileptic drugs can be impaired in case of neurodegeneration in the brain. The main aim of this review is making a reader familiar with a patomechanism of neurodegeneration as well as the current data concerning the neuro-protective potential of antiepileptic drugs. It is noteworthy that a great number of papers devoted to this problem concern animal models of neurodegeneration produced by either seizure activity or ischemia. Interestingly, there are apparent differences in the direct central effects of antiepileptic drugs in adult and young animals. Majority of antiepileptics at anticonvulsant doses produce massive apoptosis in brains of young rodents, this effect being not present in adult animals. Only topiramate required higher than anticonvulsant doses to induce apoptotic response. Neuroprotective activity in models of ischemia and epilepsy was evident for benzodiazepines (diazepam), lamotrigine, tiagabine, topiramate, and vigabatrin. Recently, topiramate has been documented to exert potent neuroprotective action in human oligodendrocytes exposed to hypoxic-ischemic damage.
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