Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling
Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling
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DOI：
10.1073/pnas.1214718110
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发表时间：
2013-01-08
影响因子：
11.1
通讯作者：
Kim, Joung-Hun
中科院分区：
文献类型：
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作者：
Budreck, Elaine C.;Kwon, Oh-Bin;Kim, Joung-Hun
尽管NMDA受体（NMDAR）的神经回路的发展和突触可塑性的关键功能，NMDAR运输的动力学的分子机制知之甚少。细胞粘附分子神经连接素-1（NL 1）可调节NMDAR依赖的突触传递和突触可塑性，但NL 1是否控制突触积聚或受体功能尚不清楚。在这里，我们提供的证据表明，NL 1调节突触后位点的NMDAR的丰度。这种功能依赖于细胞外，NL 1亚型特异性序列，促进NL 1和NMDAR GluN 1亚基之间的生物化学相互作用。我们的工作揭示了NL 1亚型特异性顺式相互作用与离子型谷氨酸受体作为控制突触特性的关键机制。
Despite the pivotal functions of the NMDA receptor (NMDAR) for neural circuit development and synaptic plasticity, the molecular mechanisms underlying the dynamics of NMDAR trafficking are poorly understood. The cell adhesion molecule neuroligin-1 (NL1) modifies NMDAR-dependent synaptic transmission and synaptic plasticity, but it is unclear whether NL1 controls synaptic accumulation or function of the receptors. Here, we provide evidence that NL1 regulates the abundance of NMDARs at postsynaptic sites. This function relies on extracellular, NL1 isoform-specific sequences that facilitate biochemical interactions between NL1 and the NMDAR GluN1 subunit. Our work uncovers NL1 isoform-specific cis-interactions with ionotropic glutamate receptors as a key mechanism for controlling synaptic properties.