Role of endonuclease G in neuronal excitotoxicity in mice.
Excitotoxicity is a process by which excitatory amino acids induce neuronal cell death. To what extent excitotoxicity is regulated by apoptotic molecules is currently unclear. We previously found that endonuclease G (EndoG) plays an important role in both normal apoptosis in vivo and in pre-implantation embryogenesis. To investigate whether EndoG participates in neuronal cell death, we compared EndoG expression and kainic acid (KA)-induced seizure behavior and excitotoxicity in EndoG+/- and wild-type mice. We found that EndoG expression in the hippocampus of EndoG+/- mice is reduced compared to that in the wild-type mice. The reduction of EndoG expression levels in the hippocampus did not result in altered KA-induced seizure severity in EndoG+/- mice compared to that in wild-type mice. However, both CA3 and CA1 pyramidal neurons in EndoG+/- mice are more resistant to KA-induced cell death than that in wild-type mice. These results indicate that reduced expression of EndoG in the hippocampi of EndoG+/- mice leads to resistance to excitotoxicity.
Wu
Yongfei
Y
Department of Cell biology, Neurobiology and Anatomy, University of Cincinnati College of Medicine, OH 45267, USA.
Dong
Mei
M
Toepfer
Nicholas J
NJ
Fan
Yunxia
Y
Xu
Ming
M
Zhang
Jianhua
J
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D004706:Endodeoxyribonucleases / Q000096:biosynthesis* / Q000235:genetics; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D006624:Hippocampus / Q000378:metabolism*; D020287:In Situ Nick-End Labeling; D007608:Kainic Acid / Q000494:pharmacology; D051379:Mice; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D021381:Protein Transport / Q000502:physiology; D012640:Seizures / Q000139:chemically induced
D018690:Excitatory Amino Acid Agonists; D004706:Endodeoxyribonucleases; C052391:endonuclease G; D007608:Kainic Acid