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

Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ phosphorylation in the hippocampus and amygdala of mice after K...

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Detalles Bibliográficos
Autores principales: Jeong, Eun Ae, Jeon, Byeong Tak, Kim, Jeong Bin, Kim, Joon Soo, Cho, Yong Woon, Lee, Dong Hoon, Kim, Hyun Joon, Kang, Sang Soo, Cho, Gyeong Jae, Choi, Wan Sung, Roh, Gu Seob
Formato: Texto
Lenguaje:English
Publicado: Korean Association of Anatomists 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998790/
https://www.ncbi.nlm.nih.gov/pubmed/21189996
http://dx.doi.org/10.5115/acb.2010.43.2.150
Descripción
Sumario:Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ 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)-14-3-3ζ and p-JNK expression was increased in the hippocampus 2 and 6 h after 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. Thus, phosphorylation of 14-3-3ζ at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.