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The potential role of mitochondrial dysfunction in seizure-associated cell death in the hippocampus and epileptogenesis

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Abstract

Epilepsy is considered one of the most common neurological disorders worldwide. The burst firing neurons associated with prolonged epileptic discharges could lead to a large number of changes with events of cascades at the cellular level. From its role as the cellular powerhouse, mitochondria also play a crucial role in the mechanisms of cell death. Emerging evidence has shown that prolonged seizures may result in mitochondrial dysfunction and increase of oxidative and nitrosative stress in the hippocampus that precede neuronal cell death and cause subsequent epileptogenesis. The selective dysfunction of mitochondrial respiratory chain Complex I has been suggested to be a biochemical hallmark of seizure-induced neuronal cell death and epileptogenesis. Therefore, protection of mitochondria from bioenergetic failure and oxidative stress in the hippocampus may open a new vista to the development of effective neuroprotective strategies against seizure-induced brain damage and to the design of novel treatment perspectives against therapy-resistant forms of epilepsy.

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Authors and Affiliations

  1. Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan

    Shang-Der Chen & Yao-Chung Chuang

  2. Center for Translational Research in Biomedical Sciences, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan

    Shang-Der Chen, Alice YW Chang & Yao-Chung Chuang

  3. Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung, Kaohsiung, 83301, Taiwan

    Yao-Chung Chuang

Authors
  1. Shang-Der Chen
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  2. Alice YW Chang
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  3. Yao-Chung Chuang
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Correspondence to Yao-Chung Chuang.

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Chen, SD., YW Chang, A. & Chuang, YC. The potential role of mitochondrial dysfunction in seizure-associated cell death in the hippocampus and epileptogenesis. J Bioenerg Biomembr 42, 461–465 (2010). https://doi.org/10.1007/s10863-010-9321-8

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  • DOI: https://doi.org/10.1007/s10863-010-9321-8

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