title: Temporal expression of AMP-activated protein kinase activation during the kainic acid-induced hippocampal cell death.
abstract: 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 Ca(2+)/calmodulin-dependent protein kinase kinasebeta (CaMKKbeta) 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.
authors.affiliation: Department of Anatomy and Neurobiology, Gyeongsang National University, Gyeongnam, Jinju, 660-751, Republic of Korea.
authors.forename: Ji Yeong
authors.initials: JY
authors.lastname: Lee
authors.forename: Beong Tak
authors.initials: BT
authors.lastname: Jeon
authors.forename: Hyun Joo
authors.initials: HJ
authors.lastname: Shin
authors.forename: Dong Hoon
authors.initials: DH
authors.lastname: Lee
authors.forename: Jae Yoon
authors.initials: JY
authors.lastname: Han
authors.forename: Hyun Joon
authors.initials: HJ
authors.lastname: Kim
authors.forename: Sang Soo
authors.initials: SS
authors.lastname: Kang
authors.forename: Gyeong Jae
authors.initials: GJ
authors.lastname: Cho
authors.forename: Wan Sung
authors.initials: WS
authors.lastname: Choi
authors.forename: Gu Seob
authors.initials: GS
authors.lastname: Roh
mesh_terms: D000091162:AMP-Activated Protein Kinase Kinases; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D054737:Calcium-Calmodulin-Dependent Protein Kinase Kinase / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology / Q000502:physiology; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D011494:Protein Kinases / Q000378:metabolism*; D012640:Seizures / Q000139:chemically induced / Q000473:pathology; D013997:Time Factors
chemical_list: D018690:Excitatory Amino Acid Agonists; D051272:Glucose Transporter Type 1; C495678:Slc2a1 protein, mouse; D011494:Protein Kinases; D054737:Calcium-Calmodulin-Dependent Protein Kinase Kinase; D000091162:AMP-Activated Protein Kinase Kinases; D053148:Caspase 3; D000103:Acetyl-CoA Carboxylase; D007608:Kainic Acid