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

Qiang Wang, Shu Ling Chiu, Eleftheria Koropouli, Ingie Hong, Sarah Mitchell, Teresa P. Easwaran, Natalie R. Hamilton, Ahleah S. Gustina, Qianwen Zhu, David D. Ginty, Richard L. Huganir, Alex L. Kolodkin

Research output: Contribution to journalArticlepeer-review

Abstract

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. Regulation of AMPA-type glutamate receptor number at synapses underlies modulation of synaptic strength during homeostatic scaling. Wang et al. show that the secreted protein semaphorin 3F (Sema3F) and its neuropilin-2/plexinA3 holoreceptor mediate homeostatic plasticity in cortical neurons.

Original languageEnglish (US)
Pages (from-to)1084-1098.e7
JournalNeuron
Volume96
Issue number5
DOIs
StatePublished - Dec 6 2017

Keywords

  • AMPA receptor
  • Neuropilin-2
  • Plexin receptor
  • Sema3F
  • homeostatic plasticity
  • semaphorin

ASJC Scopus subject areas

  • Neuroscience(all)

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