ACUTE STRESS REGULATES PHOSPHORYLATION OF N-METHYL-D-ASPARTATE RECEPTOR GLuN2B AT S1284 IN HIPPOCAMPUS
ACUTE STRESS REGULATES PHOSPHORYLATION OF N-METHYL-D-ASPARTATE RECEPTOR GLuN2B AT S1284 IN HIPPOCAMPUS
复制标题
急性应激调节海马 S1284 处 N-甲基-D-天冬氨酸受体 GLuN2B 的磷酸化
DOI：
10.1016/j.neuroscience.2017.03.029
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发表时间：
2017-05-20
期刊：
影响因子：
3.3
通讯作者：
Lu, Wen
中科院分区：
文献类型：
--
作者：
Al, Heng;Shi, Xiao-Fang;Lu, Wen
暴露于急性应激导致不同的变化，其包括在涉及应激相关病症的分子水平上的有益或有害影响。N-甲基-D-天冬氨酸受体（NMDAR）介导的信号转导被认为是应激相关精神障碍的重要参与者，也是临床治疗的有吸引力的治疗靶点。本研究利用小鼠急性应激模型，探讨了S1284对NMDAR GluN 2B亚基磷酸化水平的调节作用。我们发现，强迫游泳和急性束缚应激增加了S1284的磷酸化水平，而短暂暴露于开放场后，51284的磷酸化水平没有改变。此外，S1284的磷酸化变化被认为是细胞周期蛋白依赖性激酶抑制剂的roscovitine处理所否定。此外，S1284的磷酸化变化与强迫游泳过程中的不动时间具有良好的相关性。总之，我们的结果表明，S1284在GluN 2B的磷酸化水平的调节急性应激。(C)2017年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Exposure to acute stress leads to diverse changes, which include either beneficial or deleterious effects on molecular levels that are implicated in stress related disorders. N-methyl-D-aspartate receptor (NMDAR)mediated signalings, are thought to be vital players in stress-related mental disorders as well as attractive therapeutic targets for clinical treatment. In the present study, we utilized acute stress models in mice to explore regulation of phosphorylation level of S1284 in GIuN2B subunit of NMDAR. We found out that forced swimming and acute restraint stress increased phosphorylation level of S1284, while phosphorylation level of 51284 was unaltered after brief exposure to open field. Moreover, phosphorylation change of S1284 was negated by treatment of roscovitine which is believed to be a Cyclin-dependent kinase inhibitor. Besides, we showed well correlation of phosphorylation change of S1284 and immobility time during forced swimming. Collectively, our results demonstrated that phosphorylation level of S1284 in GIuN2B was regulated by acute stress. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.