Abstract
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 language | English |
|---|---|
| Pages (from-to) | 181-186 |
| Number of pages | 6 |
| Journal | Neuroscience Letters |
| Volume | 392 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2006 Jan 16 |
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Keywords
- Expression
- Inositol 1,4,5-trisphosphate 3-kinase A
- Kainic acid
- Rat brain
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Inhibition of rat brain inositol 1,4,5-trisphosphate 3-kinase A expression by kainic acid. / Sun, Woong; Kang, Yunhee; Kim, Il Hwan; Kim, Eun Hae; Rhyu, Im Joo; Kim, Hyun Ju; Kim, Hyun.
In: Neuroscience Letters, Vol. 392, No. 3, 16.01.2006, p. 181-186.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibition of rat brain inositol 1,4,5-trisphosphate 3-kinase A expression by kainic acid
AU - Sun, Woong
AU - Kang, Yunhee
AU - Kim, Il Hwan
AU - Kim, Eun Hae
AU - Rhyu, Im Joo
AU - Kim, Hyun Ju
AU - Kim, Hyun
PY - 2006/1/16
Y1 - 2006/1/16
N2 - 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.
AB - 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.
KW - Expression
KW - Inositol 1,4,5-trisphosphate 3-kinase A
KW - Kainic acid
KW - Rat brain
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UR - http://www.scopus.com/inward/citedby.url?scp=28444444206&partnerID=8YFLogxK
U2 - 10.1016/j.neulet.2005.09.048
DO - 10.1016/j.neulet.2005.09.048
M3 - Article
C2 - 16226375
AN - SCOPUS:28444444206
VL - 392
SP - 181
EP - 186
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 3
ER -