NGL family PSD-95-interacting adhesion molecules regulate excitatory synapse formation
NGL family PSD-95-interacting adhesion molecules regulate excitatory synapse formation
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DOI：
10.1038/nn1763
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发表时间：
2006-10-01
影响因子：
25
通讯作者：
Kim, Eunjoon
中科院分区：
文献类型：
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作者：
Kim, Seho;Burette, Alain;Kim, Eunjoon
突触细胞粘附分子（CAM）通过其跨突触和异嗜性粘附来调节突触的形成。在这里，我们表明，突触后netrin-G配体（NGL）CAMs与netrin-G CAMs的亚型特异性的方式，并通过其胞质尾部，与丰富的突触后支架突触后密度-95（PSD-95）。在培养的大鼠神经元中过表达NGL-2增加PSD-95阳性树突突起的数量。位于异源细胞或珠上的NGL-2在接触神经突中诱导功能性突触前分化。NGL-2直接聚集在树突表面膜上，诱导兴奋性突触后蛋白聚集。可溶性NGL-2的竞争性抑制减少了兴奋性突触的数量。NGL-2敲低减少兴奋性，但不抑制，突触数量和电流。这些结果表明，NGL调节兴奋性突触的形成。
Synaptic cell adhesion molecules (CAMs) regulate synapse formation through their trans-synaptic and heterophilic adhesion. Here we show that postsynaptic netrin-G ligand (NGL)CAMs associate with netrin-G CAMs in an isoform-specific manner and, through their cytosolic tail, with the abundant postsynaptic scaffold postsynaptic density-95 (PSD-95). Overexpression of NGL-2 in cultured rat neurons increased the number of PSD-95-positive dendritic protrusions. NGL-2 located on heterologous cells or beads induced functional presynaptic differentiation in contacting neurites. Direct aggregation of NGL-2 on the surface membrane of dendrites induced the clustering of excitatory postsynaptic proteins. Competitive inhibition by soluble NGL-2 reduced the number of excitatory synapses. NGL-2 knockdown reduced excitatory, but not inhibitory, synapse numbers and currents. These results suggest that NGL regulates the formation of excitatory synapses.