Neuroligin expressed in nonneuronal cells triggers presynaptic development in contacting axons
Neuroligin expressed in nonneuronal cells triggers presynaptic development in contacting axons
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DOI：
10.1016/s0092-8674(00)80877-6
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发表时间：
2000-06-09
期刊：
影响因子：
64.5
通讯作者：
Serafini, T
中科院分区：
文献类型：
--
作者：
Scheiffele, P;Fan, JH;Serafini, T
大多数神经元只与其他神经元形成突触，但对中枢神经系统突触发生的分子机制知之甚少。利用体外系统，我们证明神经胶质素-1和-2，突触后定位蛋白，可以触发突触前结构的从头形成。表达神经素的非神经元细胞可诱导接触轴突的突触前分化。这种活性可以通过添加一种可溶性的-神经素（一种神经素受体）来抑制。此外，在确定的突触前和突触后中枢神经系统神经元共培养中加入可溶性β -神经rexin，可抑制与目标神经元接触的轴突中的突触囊泡聚集。我们的研究结果表明，神经脂素是中枢神经系统突触形成和重塑过程中使用的机制的一部分。
Most neurons form synapses exclusively with other neurons, but little is known about the molecular mechanisms mediating synaptogenesis in the central nervous system. Using an in vitro system, we demonstrate that neuroligin-1 and -2, postsynaptically localized proteins, can trigger the de novo formation of presynaptic structure. Nonneuronal cells engineered to express neuroligins induce morphological and functional presynaptic differentiation in contacting axons. This activity can be inhibited by addition of a soluble version of beta-neurexin, a receptor for neuroligin. Furthermore, addition of soluble beta-neurexin to a coculture of defined pre- and postsynaptic CNS neurons inhibits synaptic vesicle clustering in axons contacting target neurons. Our results suggest that neuroligins are part of the machinery employed during the formation and remodeling of CNS synapses.