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pubmed-article:16226375pubmed:abstractTextDefects in intracellular calcium homeostasis may cause aberrant neuronal activation and subsequent neuronal death. Because inositol trisphosphate (IP(3)) regulates the release of calcium from the endoplasmic reticulum and the IP(3) kinase A isoform (IP(3)K-A) reduces intracellular IP(3), regulation of IP(3)K 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 IP(3)K-A mRNA. Since KA treatment induces aberrant neuronal activation and neuronal death, we tested whether the reduction of IP(3)K-A mRNA was required for KA-induced neuronal death. Overexpression of adenovirus-derived IP(3)K-A failed to rescue neurons from KA-induced death. Because neuronal activation by KCl in vitro is sufficient to reduce IP(3)K-A expression, we conclude that the KA-derived reduction of IP(3)K-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.lld:pubmed
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pubmed-article:16226375pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:16226375pubmed:year2006lld:pubmed
pubmed-article:16226375pubmed:articleTitleInhibition of rat brain inositol 1,4,5-trisphosphate 3-kinase A expression by kainic acid.lld:pubmed
pubmed-article:16226375pubmed:affiliationDepartment of Anatomy and Division of Brain Korea 21 Biomedical Science, Department of Anatomy, College of Medicine, Korea University, 126-1, 5-Ka, Anam-Dong, Seongbuk-Gu, Seoul 136-705, South Korea.lld:pubmed
pubmed-article:16226375pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16226375pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:16226375pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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