AP-1/σ1B-adaptin mediates endosomal synaptic vesicle recycling, learning and memory
AP-1/σ1B-adaptin mediates endosomal synaptic vesicle recycling, learning and memory
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DOI：
10.1038/emboj.2010.15
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发表时间：
2010-04-21
期刊：
影响因子：
11.4
通讯作者：
Schu, Peter
中科院分区：
文献类型：
--
作者：
Glyvuk, Nataliya;Tsytsyura, Yaroslav;Schu, Peter
突触囊泡再循环涉及AP-2/网格蛋白介导的内吞作用，但尚不清楚是否也需要内体途径。缺乏组织特异性AP-1-sigma 1B复合物的小鼠在海马突触中的突触囊泡再循环受损。普遍表达的AP-1-sigma 1A复合物介导了高尔基体网络和早期内体之间的蛋白质分选。脊椎动物表达三种σ 1亚基同种型：A、B和C。sigma 1A和sigma 1B在大脑中的表达最高。突触囊泡重组在培养的神经元从西格玛1B缺陷的小鼠是减少刺激后，和大的内体中间体积累。sigma 1B缺陷小鼠的运动协调能力下降，长期空间记忆严重受损。这些数据揭示了严重的人类X染色体连锁精神发育迟滞的分子机制。The EMBO Journal（2010）29，1318 - 1330. doi：10.1038/daj.2010.15; 2010年3月4日在线发布
Synaptic vesicle recycling involves AP-2/clathrin-mediated endocytosis, but it is not known whether the endosomal pathway is also required. Mice deficient in the tissue-specific AP-1-sigma 1B complex have impaired synaptic vesicle recycling in hippocampal synapses. The ubiquitously expressed AP-1-sigma 1A complex mediates protein sorting between the trans-Golgi network and early endosomes. Vertebrates express three sigma 1 subunit isoforms: A, B and C. The expressions of sigma 1A and sigma 1B are highest in the brain. Synaptic vesicle reformation in cultured neurons from sigma 1B-deficient mice is reduced upon stimulation, and large endosomal intermediates accumulate. The sigma 1B-deficient mice have reduced motor coordination and severely impaired long-term spatial memory. These data reveal a molecular mechanism for a severe human X-chromosome-linked mental retardation. The EMBO Journal (2010) 29, 1318-1330. doi: 10.1038/emboj.2010.15; Published online 4 March 2010