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：

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Neuropilin-2 / PlexinA3受体与GluA1相关联并介导Sema3F依赖性皮质神经元的稳态缩放。

调节突触中AMPA型谷氨酸受体（AMPAR）的数量是响应神经活动全局变化而在稳态缩放过程中控制突触强度的主要机制。我们表明，分泌的指导提示信号量3F（Sema3F）及其神经pilin-2（Npn-2）/ plexinA3（PlexA3）holoreceptor介导皮质神经元体内的稳态可塑性。Sema3F-Npn-2 / PlexA3信号对于细胞表面AMPAR稳态降尺度是必不可少的，以响应神经元活动的增加，Npn-2与AMPAR相关，而Sema3F调节这种相互作用。因此，Sema3F-Npn-2 / PlexA3信号控制突触的发展和突触可塑性。