海马体
线粒体
匹罗卡品
超微结构
癫痫
生物
化学
细胞生物学
神经科学
解剖
作者
Jing Gao,Hong Yao,Xudong Pan,Anmu Xie,Liang Zhang,Jinghui Song,Aijun Ma,Zongchao Liu
标识
DOI:10.1016/j.eplepsyres.2013.11.016
摘要
Present studies were carried out to decipher seizure-dependent changes in mitochondrial function and ultrastructure in rat hippocampus after status epilepticus (SE) induced by pilocarpine (PILO). Discernible mitochondrial ultrastructural damage was observed in the hippocampus. Enzyme assay revealed cytochrome oxidase (COX) activity significantly increased 3 h after SE, decreased 7 d and 45 d after SE, whereas succinate dehydrogenase (SDH) activity displayed no significant changes. Quantitative real-time PCR and Western blotting showed that COX III (mitochondrial-encoded) mRNA and protein level were significantly increased at 3 h, decreased to the control level on 7 d and dropped significantly on 45 d; the corresponding expression of COX IV were not changed by PILO at any time tested. The results were also supported by immunohistochemistry. Thus, our results demonstrate that dysfunction of mitochondrial complex IV respiratory enzyme and mitochondrial ultrastructural damage in the hippocampus are associated with prolonged seizure during experimental temporal lobe epilepsy and mitochondria are more vulnerable to epileptic damage.
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