Neuropilin-2/PlexinA3 Receptors Associate with GluA1 and Mediate Sema3F-Dependent Homeostatic Scaling in Cortical Neurons.,Neuron

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Neuropilin-2/PlexinA3 Receptors Associate with GluA1 and Mediate Sema3F-Dependent Homeostatic Scaling in Cortical Neurons.
Neuron ( IF 14.7 ) Pub Date : 2017-Dec-06 , DOI: 10.1016/j.neuron.2017.10.029
Qiang Wang ₁ , Shu-Ling Chiu ₂ , Eleftheria Koropouli ₁ , Ingie Hong ₂ , Sarah Mitchell ₁ , Teresa P Easwaran ₁ , Natalie R Hamilton ₁ , Ahleah S Gustina ₂ , Qianwen Zhu ₂ , David D Ginty ₃ , Richard L Huganir ₂ , Alex L Kolodkin ₁

Affiliation

Regulation of AMPA-type glutamate receptor (AMPAR) number at synapses is a major mechanism for controlling synaptic strength during homeostatic scaling in response to global changes in neural activity. We show that the secreted guidance cue semaphorin 3F (Sema3F) and its neuropilin-2 (Npn-2)/plexinA3 (PlexA3) holoreceptor mediate homeostatic plasticity in cortical neurons. Sema3F-Npn-2/PlexA3 signaling is essential for cell surface AMPAR homeostatic downscaling in response to an increase in neuronal activity, Npn-2 associates with AMPARs, and Sema3F regulates this interaction. Therefore, Sema3F-Npn-2/PlexA3 signaling controls both synapse development and synaptic plasticity.

中文翻译：

Neuropilin-2/PlexinA3 受体与 GluA1 相关并介导皮质神经元中 Sema3F 依赖性稳态缩放。

突触处 AMPA 型谷氨酸受体 (AMPAR) 数量的调节是在稳态缩放期间控制突触强度以响应神经活动的全局变化的主要机制。我们显示分泌的指导信号信号素 3F (Sema3F) 及其神经纤维蛋白 2 (Npn-2)/plexinA3 (PlexA3) 全受体介导皮质神经元的稳态可塑性。Sema3F-Npn-2/PlexA3 信号传导对于响应神经元活动增加的细胞表面 AMPAR 稳态降尺度至关重要，Npn-2 与 AMPAR 相关，Sema3F 调节这种相互作用。因此，Sema3F-Npn-2/PlexA3 信号控制突触发育和突触可塑性。

更新日期：2017-11-19

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