JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES)

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SUN Jian-ying1,FENG Yan-qiu2,CHI Zhao-fu1,WU Wei1   

  1. 1. Department of Neurology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China;2. Affiliated Hospital of Binzhou Medical College, Binzhou 256603, Shandong, China
  • Received:2006-05-09 Revised:1900-01-01 Online:2006-06-24 Published:2006-06-24
  • Contact: SUN Jian-ying

Abstract: To observe the mitochondrial damage in the hippocampal CA3 neurons during kainic acid (KA) induced status epilepticus(SE) and the neuroprotective effect of topiramate (TPM) in rats. Methods: Thirty male Wistar rats were randomly divided into TPM, KA, and NS (normal saline) groups. TPM group was pretreated with TPM for 15days. SE was induced by KA in the first two groups for 2 hours and the third group was given the same volume of NS. The seizure behaviors of rats were evaluated. Three hours later the rats were killed and the brain sections were made. We observed the neuronal damage with light microscope and the mitochondrial ultrastructure with electron microscope. Results: In KA group, SE was induced(15.3±4.6) minutes after the injection of KA, while in TPM group, (26.1±5.3) minutes, and the difference was significant (P<0.05). The damage degree of mitochondrial ultrastructure was 3.67±0.34 and 2.48±0.21 in KA and TPM groups respectively(P<0.05). Conclusion: Our results suggested that KAinduced SE can cause mitochondrial ultrastructure damage in the hippocampal neurons, and TPM has neuroprotective effect against this damage.

Key words: Status epilepticus, Lung neoplasms, Mitochondria, Ornithine decarboxylase, Ultrastructure, Gene expression , Topiramate

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