Calsyntenins function as synaptogenic adhesion molecules in concert with neurexins.
Calsyntenins function as synaptogenic adhesion molecules in concert with neurexins.
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DOI：
10.1016/j.celrep.2014.02.010
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发表时间：
2014-03-27
期刊：
影响因子：
8.8
通讯作者：
Ko J
中科院分区：
文献类型：
--
作者：
Um JW;Pramanik G;Ko JS;Song MY;Lee D;Kim H;Park KS;Südhof TC;Tabuchi K;Ko J
多种突触粘附分子控制突触的形成。在这里，我们提出calsyntenin-3/alcadein-β作为突触组织者，特异性诱导突触前分化异源突触形成试验。Calsyntenin-3（CST-3）在小鼠生后不同时期脑发育中都有高表达。同时敲除所有三个CST，但不是单独的CST-3，降低抑制性，但不是兴奋性，突触密度在培养的海马神经元。此外，在体外和体内，CSTs的敲低特异性地减少抑制性突触传递。值得注意的是，CSTs的丢失以非细胞自主的方式诱导神经元索马大小的伴随减少。此外，α-neurexins（α-Nrxs）被亲和纯化为CST-3复合物的成分，参与CST-3介导的突触前分化。然而，CST-3不直接结合Nrxs。综合来看，这些数据表明，这三个CST冗余调节抑制性突触的形成，抑制性突触的功能，和神经元的发展与Nrxs一致。
Multiple synaptic adhesion molecules govern synapse formation. Here, we propose calsyntenin-3/alcadein-β as a synapse organizer that specifically induces presynaptic differentiation in heterologous synapse-formation assays. Calsyntenin-3 (CST-3) was highly expressed during various postnatal periods of mouse brain development. The simultaneous knockdown of all three CSTs, but not CST-3 alone, decreased inhibitory, but not excitatory, synapse densities in cultured hippocampal neurons. Moreover, the knockdown of CSTs specifically reduced inhibitory synaptic transmission in vitro and in vivo. Remarkably, the loss of CSTs induced a concomitant decrease in neuron soma size in a non-cell-autonomous manner. Furthermore, α-neurexins (α-Nrxs) were affinity-purified as components of a CST-3 complex involved in CST-3-mediated presynaptic differentiation. However, CST-3 did not directly bind to Nrxs. Viewed together, these data suggest that the three CSTs redundantly regulate inhibitory synapse formation, inhibitory synapse function, and neuron development in concert with Nrxs.
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