Microcystin-LR inhibited hippocampal long-term potential via regulation of the glycogen synthase kinase-3 beta pathway
文献类型: 外文期刊
作者: Wang, Jianghua 1 ; Lin, Fankai 2 ; Cai, Fei 3 ; Yan, Wei 4 ; Zhou, Qiong 1 ; Xie, Liqiang 5 ;
作者机构: 1.Huazhong Agr Univ, Coll Fisheries, Wuhan 430070, Peoples R China
2.Beijing Inst Technol, Sch Life Sci, Beijing 100081, Peoples R China
3.Xianning Univ, Dept Pharmacol, Coll Med, Xianning 437100, Peoples R China
4.Hubei Acad Agr Sci, Inst Agr Qual Stand & Testing Technol, Wuhan 430064, Peoples R China
5.Chinese Acad Sci, State Key Lab Lake Sci & Environm, Nanjing Inst Geog & Limnol, Nanjing 210008, Peoples R China
关键词: Microcystin-LR;Long-term potential;Hippocampus;Glycogen synthase kinase-3 beta
期刊名称:CHEMOSPHERE ( 影响因子:7.086; 五年影响因子:6.956 )
ISSN: 0045-6535
年卷期: 2013 年 93 卷 2 期
页码:
收录情况: SCI
摘要: We previously demonstrated that Cyanobacteria-derived microcystin-LR (MCLR) is able to induce cognitive dysfunction, but the mechanism is not understood. Long-term potential (LTP) in hippocampus is regarded as an important cellular mechanism of learning and memory. Here, the aim of this study was to evaluate the role of MCLR in LTP of hippocampal dentate gyrus (DG) by in vivo electrophysiological recording. We found that MCLR could suppress the induction of LTP in rat hippocampus, whereas simultaneous inhibition of glycogen synthase kinase-3 beta (GSK-3 beta) by LiCI or SB216763 attenuated the LTP impairments by MCLR. Furthermore, a decrease of the phosphorylated level at Ser9 of GSK-3 beta was observed by western blotting after intracerebroventricular (ICV) injection of MCLR, indicating GSK-3 beta was activated by MCLR. In addition, we showed that ICV administration of MCLR slightly stimulated activity of protein phosphatases (PPs) in the brain, which might activate GSK-3 beta via dephosphorylation of Ser9 site. Taken together, these findings demonstrated that GSK-3 beta plays a crucial role in regulating MCLR-induced cognitive deficit. (C) 2013 Elsevier Ltd. All rights reserved.
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