转铁蛋白受体控制AMPA受体转运效率和突触可塑性。
Transferrin Receptor Controls AMPA Receptor Trafficking Efficiency and Synaptic Plasticity.
作者信息
Liu Ke, Lei Run, Li Qiong, Wang Xin-Xin, Wu Qian, An Peng, Zhang Jianchao, Zhu Minyan, Xu Zhiheng, Hong Yang, Wang Fudi, Shen Ying, Li Hongchang, Li Huashun
机构信息
West China Developmental &Stem Cell Institute, West China Second Hospital, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan 610041, China.
Shenzhen Key Laboratory for Molecular Biology of Neural Development, Laboratory of Developmental and Regenerative Biology, Institute of Biomedicine &Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055, China.
出版信息
Sci Rep. 2016 Feb 16;6:21019. doi: 10.1038/srep21019.
Transferrin receptor (TFR) is an important iron transporter regulating iron homeostasis and has long been used as a marker for clathrin mediated endocytosis. However, little is known about its additional function other than iron transport in the development of central nervous system (CNS). Here we demonstrate that TFR functions as a regulator to control AMPA receptor trafficking efficiency and synaptic plasticity. The conditional knockout (KO) of TFR in neural progenitor cells causes mice to develop progressive epileptic seizure, and dramatically reduces basal synaptic transmission and long-term potentiation (LTP). We further demonstrate that TFR KO remarkably reduces the binding efficiency of GluR2 to AP2 and subsequently decreases AMPA receptor endocytosis and recycling. Thus, our study reveals that TFR functions as a novel regulator to control AMPA trafficking efficiency and synaptic plasticity.
转铁蛋白受体（TFR）是一种调节铁稳态的重要铁转运蛋白，长期以来一直被用作网格蛋白介导的内吞作用的标志物。然而，除了在中枢神经系统（CNS）发育过程中的铁转运功能外，人们对其其他功能知之甚少。在这里，我们证明TFR作为一种调节因子，可控制AMPA受体的转运效率和突触可塑性。神经祖细胞中TFR的条件性敲除（KO）导致小鼠出现进行性癫痫发作，并显著降低基础突触传递和长时程增强（LTP）。我们进一步证明，TFR敲除显著降低了GluR2与AP2的结合效率，随后减少了AMPA受体的内吞作用和再循环。因此，我们的研究表明，TFR作为一种新型调节因子，可控制AMPA的转运效率和突触可塑性。
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