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http://dx.doi.org/10.5115/acb.2010.43.2.150

Phosphorylation of 14-3-$3{\zeta}$ at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity  

Jeong, Eun-Ae (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Jeon, Byeong-Tak (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Kim, Jeong-Bin (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Kim, Joon-Soo (Department of Neurosurgery, Masan Samsung Hospital, Sungkyunkwan University School of Medicine)
Cho, Yong-Woon (Department of Neurosurgery, Masan Samsung Hospital, Sungkyunkwan University School of Medicine)
Lee, Dong-Hoon (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Kim, Hyun-Joon (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Kang, Sang-Soo (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Cho, Gyeong-Jae (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Choi, Wan-Sung (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Roh, Gu-Seob (Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine)
Publication Information
Anatomy and Cell Biology / v.43, no.2, 2010 , pp. 150-156 More about this Journal
Abstract
Oxidative stress-induced cell death leads to phosphorylation of 14-3-$3{\zeta}$ at serine 58. 14-3-$3{\zeta}$ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-$3{\zeta}$ phosphorylation in the hippocampus and amygdala of mice after 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-$3{\zeta}$ and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-$3{\zeta}$-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-$3{\zeta}$ at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.
Keywords
Kainic acid; 14-3-$3{\zeta}$; hippocampus; amygdala; neurodegeneration;
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