Synaptic P-Rex1 signaling regulates hippocampal long-term depression and autism-like social behavior
文献类型：期刊论文
| 作者 | Li J1,2,3; Chai A4,5,6; Wang LF1,2,3; Ma YL1,2,3; Wu ZL1,2,3; Yu H1,2,3; Mei LW1,2,3; Lu L1,2,3; Zhang C7,8; Yue WH1,2,3 |
| 刊名 | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
 |
| 出版日期 | 2015 |
| 卷号 | 112期号:50页码:E6964-6972 |
| 通讯作者 | lxu@vip.163.com ; daizhang@bjmu.edu.cn |
| 合作状况 | 其它 |
| 英文摘要 | Autism spectrum disorders (ASDs) are a group of highly inheritable mental disorders associated with synaptic dysfunction, but the underlying cellular and molecular mechanisms remain to be clarified. Here we report that autism in Chinese Han population is associated with genetic variations and copy number deletion of P-Rex1 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 1). Genetic deletion or knockdown of P-Rex1 in the CA1 region of the hippocampus in mice resulted in autism-like social behavior that was specifically linked to the defect of long-term depression (LTD) in the CA1 region through alteration of AMPA receptor endocytosis mediated by the postsynaptic PP1α (protein phosphase 1α)-P-Rex1-Rac1 (Ras-related C3 botulinum toxin substrate 1) signaling pathway. Rescue of the LTD in the CA1 region markedly alleviated autism-like social behavior. Together, our findings suggest a vital role of P-Rex1 signaling in CA1 LTD that is critical for social behavior and cognitive function and offer new insight into the etiology of ASDs. |
| 收录类别 | SCI |
| 资助信息 | This work was supported by Grants 2010CB833905 and 2013CB835103 from Program 973 of the Ministry of Science and Technology of China; by Grants 91232305, 81471360, 81222017, 81471383, 81221002, and 81501183 from the National Natural Science Foundation of China; and by Shenzhen Basic Research Grant JC201104220331A. |
| 语种 | 英语 |
| 源URL | [http://159.226.149.26:8080/handle/152453/9499]  |
| 专题 | 昆明动物研究所_学习记忆的分子神经机制 昆明动物研究所_动物模型与人类重大疾病机理重点实验室 |
| 作者单位 | 1.Institute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China 2.National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China 3.Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China 4.Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China 5.Kunming Institute of Zoology/The Chinese University of Hong Kong Joint Laboratory of Bioresources and Molecular Research in Common Disease, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China 6.Laboratory of Learning and Memory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China 7.School of Life Sciences, Peking University, Beijing 100871, China 8.Peking University-International Data Group/McGovern Institute for Brain Research, Peking University, Beijing 100871, China 9.Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China 10.Shenzhen Key Laboratory for Neuronal Structural Biology, Shenzhen Peking University-Hong Kong University of Science and Technology Medical Center, Shenzhen, 518035, China |
| 推荐引用方式 GB/T 7714 | Li J,Chai A,Wang LF,et al. Synaptic P-Rex1 signaling regulates hippocampal long-term depression and autism-like social behavior[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,2015,112(50):E6964-6972. |
| APA | Li J.,Chai A.,Wang LF.,Ma YL.,Wu ZL.,...&Zhang D[*].(2015).Synaptic P-Rex1 signaling regulates hippocampal long-term depression and autism-like social behavior.PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,112(50),E6964-6972. |
| MLA | Li J,et al."Synaptic P-Rex1 signaling regulates hippocampal long-term depression and autism-like social behavior".PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 112.50(2015):E6964-6972. |
入库方式： OAI收割
来源：昆明动物研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。