突触发生
突触后电位
平行光纤
兴奋性突触后电位
神经鞘素
神经科学
生物
致电离效应
浦肯野细胞
细胞生物学
谷氨酸受体
小脑
受体
化学
生物化学
抑制性突触后电位
作者
J. Elegheert,Wataru Kakegawa,Jordan E. Clay,Natalie F. Shanks,Ester Behiels,Keiko Matsuda,Kazuhisa Kohda,Eriko Miura,Maxim Rossmann,Nikolaos Mitakidis,Junko Motohashi,Veronica T. Chang,Christian Siebold,Ingo H. Greger,Terunaga Nakagawa,Michisuke Yuzaki,A. Radu Aricescu
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2016-07-15
卷期号:353 (6296): 295-299
被引量:119
标识
DOI:10.1126/science.aae0104
摘要
Ionotropic glutamate receptor (iGluR) family members are integrated into supramolecular complexes that modulate their location and function at excitatory synapses. However, a lack of structural information beyond isolated receptors or fragments thereof currently limits the mechanistic understanding of physiological iGluR signaling. Here, we report structural and functional analyses of the prototypical molecular bridge linking postsynaptic iGluR δ2 (GluD2) and presynaptic β-neurexin 1 (β-NRX1) via Cbln1, a C1q-like synaptic organizer. We show how Cbln1 hexamers "anchor" GluD2 amino-terminal domain dimers to monomeric β-NRX1. This arrangement promotes synaptogenesis and is essential for D: -serine-dependent GluD2 signaling in vivo, which underlies long-term depression of cerebellar parallel fiber-Purkinje cell (PF-PC) synapses and motor coordination in developing mice. These results lead to a model where protein and small-molecule ligands synergistically control synaptic iGluR function.
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