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 language | English (US) |
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Pages (from-to) | 1084-1098.e7 |
Journal | Neuron |
Volume | 96 |
Issue number | 5 |
DOIs | |
State | Published - Dec 6 2017 |
Keywords
- AMPA receptor
- Neuropilin-2
- Plexin receptor
- Sema3F
- homeostatic plasticity
- semaphorin
ASJC Scopus subject areas
- Neuroscience(all)