Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling.

Abstract

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.

DOI: 10.1073/pnas.1214718110
05010015020132014201520162017
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@article{Budreck2013Neuroligin1CS, title={Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling.}, author={Elaine C Budreck and Oh-Bin Kwon and Jung Hoon Jung and Stephane Baudouin and Albert Thommen and Hye-Sun Kim and Yugo Fukazawa and Harumi Harada and Katsuhiko Tabuchi and Ryuichi Shigemoto and Peter Scheiffele and Joung-Hun Kim}, journal={Proceedings of the National Academy of Sciences of the United States of America}, year={2013}, volume={110 2}, pages={725-30} }