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
- 정은애; 전병탁; 김정빈; 김준수; 최용원; 이동훈; 김현준; 강상수; 조경제; 최완성; 노구섭
- 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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Collections - College of Medicine > Department of Medicine > Journal Articles
- 의학계열 > 의학과 > Journal Articles

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