Mitochondrial dysfunction has been identified as one potential cause of epileptic seizures. Impaired mitochondrial function has been reported for the seizure focus of patients with temporal lobe epilepsy and Ammon's horn sclerosis and of adult and immature animal models of epilepsy. Since mitochondrial oxidative phosphorylation provides the major source of ATP in neurons and mitochondria participate in cellular Ca(2+) homeostasis and generation of reactive oxygen species, their dysfunction strongly affects neuronal excitability and synaptic transmission. Therefore, mitochondrial dysfunction is proposed to be highly relevant for seizure generation. Additionally, mitochondrial dysfunction is known to trigger neuronal cell death, which is a prominent feature of therapy-resistant epilepsy. For this reason mitochondria have to be considered as promising targets for neuroprotective strategies in epilepsy.

Department of Developmental Epileptology Institute of Physiology Academy of Sciences of the Czech Republic Prague Czech Republic

Citace poskytuje Crossref.org

Epilepsy Research in the Institute of Physiology of the Czech Academy of Sciences in Prague

Protective Effect of Sulforaphane on Oxidative Stress and Mitochondrial Dysfunction Associated with Status Epilepticus in Immature Rats

Sulforaphane Ameliorates Metabolic Changes Associated With Status Epilepticus in Immature Rats

Treatment With Resveratrol Ameliorates Mitochondrial Dysfunction During the Acute Phase of Status Epilepticus in Immature Rats

1,2,4-Triazole-based anticonvulsant agents with additional ROS scavenging activity are effective in a model of pharmacoresistant epilepsy

The evaluation of oxidative damage of DNA after poisoning with nerve agents

Bioenergetic Mechanisms of Seizure Control

Effect of Resveratrol on Oxidative Stress and Mitochondrial Dysfunction in Immature Brain during Epileptogenesis

Status Epilepticus in Immature Rats Is Associated with Oxidative Stress and Mitochondrial Dysfunction