Involvement of Scn1b and Kcna1 ion channels in audiogenic seizures and PTZ-induced epilepsy

Xianchun Li, Hui Kuang, Nan Jiang, Yinghe Hu

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

We have undertaken chemical genetic approach using Qingyangshenylycosides (QYS), a natural product compound, to explore the molecular mechanisms underlying different types of epilepsy models. Two animal models were used for these studies, i.e., audiogenic seizure (AGS) and pentylenetetrazol (PTZ)-induced generalized epilepsy in DBA/2J mice. We show that the latency of AGS is prolonged and the severity of seizures (the percentages of the tonus, Tonus_%) is reduced in the QYS-treated animals. These results indicate that QYS has anticonvulsant effect on the AGS model. However, we find that administration of QYS has an opposite effects on PTZ-induced generalized epilepsy. Both the latency of the generalized epilepsy and the latency of death are decreased after QYS treatment in PTZ-induced epilepsy. We examine the molecular basis of the distinct roles of QYS in these two epilepsy models by using gene expression data. Our results show that a voltage-gated sodium channel (Scn1b) and a voltage-gated potassium channel (Kcna1) are differentially expressed in AGS and PTZ-induced epilepsy models as well as in QYS-treated animals. Our results demonstrate that a chemical genetic approach may help to reveal both the molecular mechanisms of different epilepsies and the mechanism of action of the antiepileptic drugs.

Original languageEnglish (US)
Pages (from-to)155-163
Number of pages9
JournalEpilepsy Research
Volume66
Issue number1-3
DOIs
Publication statusPublished - Jan 1 2005

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Keywords

  • Anticonvulsant
  • Audiogenic seizure
  • Epilepsy
  • Pentylenetatrazol
  • Qingyangshenylycosides

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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