Anatomy and Cell Biology

  • 제43권2호
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  • Pages.150-156
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  • 2010
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  • 2093-3665(pISSN)
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  • 2093-3673(eISSN)
대한해부학회 (Korean Association of Anatomists)
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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)
  • 투고 : 2010.04.28
  • 심사 : 2010.05.31
  • 발행 : 2010.06.30
⟨ 이전 논문 다음 논문 ⟩

초록

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.

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과제정보

연구 과제 주관 기관 : National Research Foundation (NRF) of Korea

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