Modulation of mGluR-Dependent MAP1B Translation and AMPA Receptor Endocytosis by MicroRNA miR-146a-5p

被引：49
作者：
Chen, Ying-Lin [1 ,2 ,3 ]
Shen, Che-Kun James [1 ,2 ,3 ]
机构：
[1] Natl Yang Ming Univ, Dept Life Sci, Taipei 112, Taiwan
[2] Natl Yang Ming Univ, Inst Genome Sci, Taipei 112, Taiwan
[3] Acad Sinica, Inst Mol Biol, Taipei 115, Taiwan
来源：
JOURNAL OF NEUROSCIENCE | 2013年 / 33卷 / 21期
关键词：
LONG-TERM DEPRESSION; FRAGILE-X-SYNDROME; PROTEIN; 1B; GLUTAMATE RECEPTORS; SYNAPTIC PLASTICITY; MENTAL-RETARDATION; CORTICAL-NEURONS; RETT-SYNDROME; EXPRESSION; BIOGENESIS;
D O I：
10.1523/JNEUROSCI.5210-12.2013
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The translation of dendritic microtubule-associated protein 1B (MAP1B) is exaggerated upon group I mGluR activation leading to AMPA receptor (AMPAR) endocytosis and consequent long-term depression. However, the mechanisms of regulation of MAP1B protein synthesis in the mature dendrites remain unclear. Here we have identified miR-146a-5p that targets the 3' UTR of MAP1B mRNA and represses its translation. Inhibition of the endogenous miR-146a-5p in mouse cultured hippocampal neurons triggers an increase of the dendritic MAP1B protein as well as the internalization of AMPARs, resulting in a decline in synaptic transmission. Conversely, enforced expression of miR-146a-5p inhibits MAP1B translation and attenuates group I mGluR-induced AMPAR endocytosis. Moreover, siRNA-mediated knockdown of MAP1B recovers the impairment of synaptic transmission caused by inhibition of miR-146a-5p. These results reveal that miR-146a-5p modulates the synaptic plasticity via repression of MAP1B protein synthesis.
引用
收藏
页码：9013 / 9020
页数：8
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