Transferrin Receptor Controls AMPA Receptor Trafficking Efficiency and Synaptic Plasticity.
Transferrin Receptor Controls AMPA Receptor Trafficking Efficiency and Synaptic Plasticity.
复制标题
转铁蛋白受体控制 AMPA 受体运输效率和突触可塑性。
DOI：
10.1038/srep21019
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发表时间：
2016-02-16
影响因子：
4.6
通讯作者：
Li H
中科院分区：
文献类型：
--
作者：
Liu K;Lei R;Li Q;Wang XX;Wu Q;An P;Zhang J;Zhu M;Xu Z;Hong Y;Wang F;Shen Y;Li H;Li H
转铁蛋白受体（TFR）是调节铁稳态的重要铁转运蛋白，长期以来一直用作网格蛋白介导的内吞作用的标记。然而，除了铁中枢神经系统（CNS）的发展中，除了铁运输以外，其其他功能知之甚少。在这里，我们证明TFR是控制AMPA受体运输效率和突触可塑性的调节剂。神经祖细胞中TFR的条件敲除（KO）导致小鼠发育性癫痫发作，并大大减少基础突触传播和长期增强（LTP）。我们进一步证明，TFR KO明显降低了GLUR2与AP2的结合效率，并随后降低了AMPA受体内吞作用和回收利用。因此，我们的研究表明，TFR是控制AMPA运输效率和突触可塑性的新型调节剂。
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.
DOI：
10.1007/s00259-011-1871-4
发表时间：
2011-10
影响因子：
9.1
作者：
Quan, Qimeng;Yang, Min;Gao, Haokao;Zhu, Lei;Lin, Xin;Guo, Ning;Zhang, Guixiang;Eden, Henry S.;Niu, Gang;Chen, Xiaoyuan
通讯作者：
Chen, Xiaoyuan