期刊
TOXICOLOGY LETTERS
卷 193, 期 2, 页码 189-193出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2010.01.008
关键词
Hyperphosphorylation; Brain; Tau; Ketamine abuse; Alzheimer's disease; Neurodegeneration
类别
资金
- Beat Drugs Fund Association, Hong Kong Government [080048]
Ketamine, a non-competitive antagonist at the glutamatergic N-methyl-D-aspartate (NMDA) receptor, might impair memory function of the brain. Loss of memory is also a characteristic of aging and Alzheimer's disease. Hyperphosphorylation of tau is an early event in the aging process and Alzheimer's disease. Therefore, we aimed to find out whether long-term ketmaine administration is related to hyperphosphorylation of tau or not in the brains of mice and monkeys. Results showed that after 6 months' administration of ketamine, in the prefrontal and entorhinal cortical sections of mouse and monkey brains, there were significant increases of positive sites for the hyperphosphorylated tau protein as compared to the control animals receiving no ketamine administration. Furthermore, about 15% of hyperphosphorylated tau positive cells were also positively labeled by terminal dUTP nick end labeling (TUNEL) indicating there might be a relationship between hyperphosphorylation of tau and apoptosis. Therefore, the long-term ketamine toxicity might involve neurodegenerative process similar to that of aging and/or Alzheimer's disease. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据