| Literature DB >> 29154130 |
Qiang Wang1, Shu-Ling Chiu2, Eleftheria Koropouli1, Ingie Hong2, Sarah Mitchell1, Teresa P Easwaran1, Natalie R Hamilton1, Ahleah S Gustina2, Qianwen Zhu2, David D Ginty3, Richard L Huganir2, Alex L Kolodkin4.
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.Entities:
Keywords: AMPA receptor; Neuropilin-2; Plexin receptor; Sema3F; homeostatic plasticity; semaphorin
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Year: 2017 PMID: 29154130 PMCID: PMC5726806 DOI: 10.1016/j.neuron.2017.10.029
Source DB: PubMed Journal: Neuron ISSN: 0896-6273 Impact factor: 17.173