Temporal expression of AMP-activated protein kinase activation during the kainic acid-induced hippocampal cell death

被引:22
作者
Lee, Ji Yeong [1 ]
Jeon, Beong Tak [1 ]
Shin, Hyun Joo [1 ]
Lee, Dong Hoon [1 ]
Han, Jae Yoon [1 ]
Kim, Hyun Joon [1 ]
Kang, Sang Soo [1 ]
Cho, Gyeong Jae [1 ]
Choi, Wan Sung [1 ]
Roh, Gu Seob [1 ]
机构
[1] Gyeongsang Natl Univ, Sch Med, Med Res Ctr Neural Dysfunct, Inst Hlth Sci,Dept Anat & Neurobiol, Gyeongnam 660751, Jinju, South Korea
基金
英国医学研究理事会;
关键词
Kainic acid; Seizure; AMP-activated protein kinase; Hippocampus; Mice; NEUROBLASTOMA-CELLS; SKELETAL-MUSCLE; BETA-CELLS; GLUCOSE; STRESS; RAT; APOPTOSIS; NEURONS; CALCIUM; INJURY;
D O I
10.1007/s00702-008-0158-9
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Kainic acid (KA)-induced seizure induces the hippocampal cell death. There are reports that AMP-activated protein kinase (AMPK), which is an important regulator of energy homeostasis of cells, has been proposed as apoptotic molecule. In this study, we investigated the altered expression of AMPK cascade in the hippocampus of mice during KA-induced hippocampal cell death. Mice were killed at 2, 6, 24 or 48 h after KA (30 mg/kg) injection. Histological evaluation of KA-treated hippocampus revealed hippocampal cell death first at 6 h and appearing prominently by 48 h after KA injection. Immunoreactivity of Ca2+/calmodulin-dependent protein kinase kinase beta (CaMKK beta) was increased after KA treatment. In Western blot analysis, AMPK activation was increased 2 h after KA treatment. The proteins of downstream AMPK, including those of glucose transporter1 (GLUT1) and phosphorylation of Acetyl CoA Carboxylase (ACC) were increased in the hippocampus after KA treatment. These results indicate that sustained AMPK activation might be a mechanism by which KA-induced seizure causes hippocampal cell death of mice.
引用
收藏
页码:33 / 40
页数:8
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