Bridging the Synaptic Cleft: Lessons from Orphan Glutamate Receptors
Bridging the Synaptic Cleft: Lessons from Orphan Glutamate Receptors
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DOI：
10.1126/scisignal.3136pe28
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发表时间：
2010-08-24
影响因子：
7.3
通讯作者：
Hollmann, Michael
中科院分区：
文献类型：
--
作者：
Schmid, Sabine M.;Hollmann, Michael
对于神经元来说，信号必须在它们的接触点跨越细胞与细胞之间的距离。在中枢神经系统中主要的细胞-细胞接触处，即化学突触，突触间隙的跨度约为20纳米。为了跨越这段距离发出信号，突触前神经元分泌一种可扩散的神经递质，由突触后神经元上的受体检测到。虽然这种信号机制已经成为常识，但仍然不清楚突触在不立即使用时如何维持。新的证据揭示了大自然是如何在小脑的一种特殊类型的突触上解决这个问题的：三个老熟人在裂缝上架起了桥梁。离子型谷氨酸受体GluD 2构成突触后锚，其通过突触前分泌的可溶性因子（C1 q蛋白家族的一个成员，名为Cbln 1）与突触前锚神经毒素间接相互作用。这三个人合作，使突触前和突触后两侧对齐。
For neurons to communicate, signals must cross the cell-to-cell distance at their points of contact. At the predominant cell-cell contact in the central nervous system, the chemical synapse, the synaptic cleft spans roughly 20 nanometers. To signal across this distance, the presynaptic neuron secretes a diffusible neurotransmitter, which is detected by receptors on the postsynaptic neuron. Although this signaling mechanism has become common knowledge, it remains unclear how synapses are maintained when they are not in immediate use. New evidence reveals how Nature solved this problem at a particular type of synapse in the cerebellum: Three old acquaintances bridge the cleft. The ionotropic glutamate receptor GluD2 constitutes the postsynaptic anchor that indirectly interacts with the presynaptic anchor neurexin through a presynaptically secreted soluble factor, a member of the C1q protein family named Cbln1. This trio collaborates to align pre- and postsynaptic sides.