Phosphorylation of 14-3-3zeta at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity.
10.5115/acb.2010.43.2.150
- Author:
Eun Ae JEONG
1
;
Byeong Tak JEON
;
Jeong Bin KIM
;
Joon Soo KIM
;
Yong Woon CHO
;
Dong Hoon LEE
;
Hyun Joon KIM
;
Sang Soo KANG
;
Gyeong Jae CHO
;
Wan Sung CHOI
;
Gu Seob ROH
Author Information
1. Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine, Jinju, Korea. anaroh@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Kainic acid;
14-3-3zeta;
hippocampus;
amygdala;
neurodegeneration
- MeSH:
Amygdala;
Animals;
Cell Death;
Fluoresceins;
Hippocampus;
In Situ Nick-End Labeling;
Kainic Acid;
Mice;
Neurons;
Phosphorylation;
Seizures;
Serine
- From:Anatomy & Cell Biology
2010;43(2):150-156
- CountryRepublic of Korea
- Language:English
-
Abstract:
Oxidative stress-induced cell death leads to phosphorylation of 14-3-3zeta at serine 58. 14-3-3zeta is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3zeta phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after 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)-14-3-3zeta and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3zeta-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3zeta at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.
