| Preservation of mitochondrial integrity and energy metabolism during experimental status epilepticus leads to neuronal apoptotic cell death in the hippocampus of the rat. | |
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MedLine Citation:
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PMID: 19375359 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Status epilepticus results in mitochondrial damage or dysfunction and preferential neuronal cell loss in the hippocampus. Since a critical determinant of the eventual cell death fate resides in intracellular ATP concentration, we investigated whether mitochondrial integrity and level of energy metabolism are related with apoptotic cell death in specific hippocampal neuronal populations. A kainic acid (KA)-induced experimental temporal lobe status epilepticus model was used. Qualitative and quantitative analysis of DNA fragmentation, TUNEL immunohistochemistry, double immunofluorescence staining for activated caspase-3, electron microscopy or measurement of ATP level in the bilateral hippocampus was carried out 1, 3 or 7 days after microinjection unilaterally of a low dose of KA (0.5 nmol) into the CA3 hippocampal subfield. Characteristic biochemical (DNA fragmentation), histochemical (TUNEL or activated caspase-3 staining) or ultrastructural (electron microscopy) features of apoptotic cell death were presented bilaterally in the hippocampus 7 days after the elicitation of sustained hippocampal seizure activity by microinjection of KA into the unilateral CA3 subfield. At the same time, CA3 or CA1 subfield on either side manifested a maintained ATP level; alongside relatively intact mitochondria, rough endoplasmic reticulum, Golgi apparatus or cytoplasmic membrane in hippocampal neurons that exhibited ultrastructural features of apoptotic cell death. Our results demonstrated that preserved mitochondrial ultrastructural integrity and maintained energy metabolism during experimental temporal lobe status epilepticus is associated specifically with apoptotic, not necrotic, cell death in hippocampal CA3 or CA1 neurons. |
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Authors:
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Yao-Chung Chuang; Jui-Wei Lin; Shang-Der Chen; Tsu-Kung Lin; Chia-Wei Liou; Cheng-Hsien Lu; Wen-Neng Chang |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-04-17 |
Journal Detail:
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Title: Seizure : the journal of the British Epilepsy Association Volume: 18 ISSN: 1532-2688 ISO Abbreviation: Seizure Publication Date: 2009 Jul |
Date Detail:
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Created Date: 2009-06-08 Completed Date: 2009-09-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9306979 Medline TA: Seizure Country: England |
Other Details:
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Languages: eng Pagination: 420-8 Citation Subset: IM |
Affiliation:
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Department of Neurology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan. ycchuang@adm.cgmh.org.tw |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Analysis of Variance Animals Apoptosis / drug effects, physiology* Caspase 3 / metabolism DNA Fragmentation / drug effects Disease Models, Animal Energy Metabolism / physiology* Excitatory Amino Acid Agonists / pharmacology Hippocampus / drug effects, pathology* In Situ Nick-End Labeling / methods Kainic Acid / pharmacology Male Microscopy, Electron, Transmission / methods Mitochondria / pathology*, ultrastructure Neurons / drug effects, pathology*, ultrastructure Phosphopyruvate Hydratase / metabolism Rats Rats, Sprague-Dawley Status Epilepticus* / chemically induced, metabolism, pathology, physiopathology Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Excitatory Amino Acid Agonists; 487-79-6/Kainic Acid; 56-65-5/Adenosine Triphosphate; EC 3.4.22.-/Caspase 3; EC 4.2.1.11/Phosphopyruvate Hydratase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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