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Phosphorylation of 14-3-3ζ at serine 58 and neurodegeneration following kainic acid-induced excitotoxicityPhosphorylation of 14-3-3ζ at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity

Other Titles
Phosphorylation of 14-3-3ζ at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity
Authors
정은애전병탁김정빈김준수최용원이동훈김현준강상수조경제최완성노구섭
Issue Date
Jun-2010
Publisher
대한해부학회
Keywords
Kainic acid; 14-3-3ζ; hippocampus; amygdala; neurodegeneration
Citation
Anatomy and Cell Biology, v.43, no.2, pp 150 - 156
Pages
7
Indexed
KCI
Journal Title
Anatomy and Cell Biology
Volume
43
Number
2
Start Page
150
End Page
156
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/77582
ISSN
2093-3665
2093-3673
Abstract
Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at signifi cant levels in cerebrospinal fl uid aft er kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ phosphorylation in the hippocampus and amygdala of mice aft er KA treatment. Mice were killed at 2, 6, 24, or 48 h aft er KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3ζ and p-JNK expression was increased in the hippocampus 2 and 6 h aft er KA treatment, respectively. In immunohistochemical analysis, p-14-3-3ζ-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Th us, phosphorylation of 14-3-3ζ at serine 58may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.
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