Journal
ANATOMY & CELL BIOLOGY
Volume 43, Issue 2, Pages 150-156Publisher
MEDRANG
DOI: 10.5115/acb.2010.43.2.150
Keywords
Kainic acid; 14-3-3 zeta; hippocampus; amygdala; neurodegeneration
Categories
Funding
- National Research Foundation (NRF) of Korea [R13-2005-012-01001-0, 2009-0064327]
- National Research Foundation of Korea [2009-0064327, R13-2005-012-01001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Ask authors/readers for more resources
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 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)-14-3-3 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available