Inhibition of rat brain inositol 1,4,5-trisphosphate 3-kinase A expression by kainic acid

Woong Sun, Yunhee Kang, Il Hwan Kim, Eun Hae Kim, Im Joo Rhyu, Hyun Ju Kim, Hyun Kim

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


Defects in intracellular calcium homeostasis may cause aberrant neuronal activation and subsequent neuronal death. Because inositol trisphosphate (IP3) regulates the release of calcium from the endoplasmic reticulum and the IP3 kinase A isoform (IP3K-A) reduces intracellular IP3, regulation of IP3K could be involved in neuronal activation and/or neuronal death. In this study, we found that kainic acid (KA) treatment in vitro and in vivo reduced the level of IP3K-A mRNA. Since KA treatment induces aberrant neuronal activation and neuronal death, we tested whether the reduction of IP3K-A mRNA was required for KA-induced neuronal death. Overexpression of adenovirus-derived IP 3K-A failed to rescue neurons from KA-induced death. Because neuronal activation by KCl in vitro is sufficient to reduce IP3K-A expression, we conclude that the KA-derived reduction of IP3K-A expression is due to the aberrant neuronal activation, and the reduction in the IP3K-A mRNA level is not required for the toxic effect of KA.

Original languageEnglish
Pages (from-to)181-186
Number of pages6
JournalNeuroscience Letters
Issue number3
Publication statusPublished - 2006 Jan 16

Bibliographical note

Funding Information:
This work was supported by grants M10218020001-02B2002-00210 and M103KV010018-03K2201-01821 from the Korean Ministry of Science and Technology. A part of this work was technically supported by the core facility service of the 21C Frontier Brain Research Center.


  • Expression
  • Inositol 1,4,5-trisphosphate 3-kinase A
  • Kainic acid
  • Rat brain

ASJC Scopus subject areas

  • General Neuroscience


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