Journal
NEURON
Volume 96, Issue 5, Pages 1084-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2017.10.029
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Funding
- NIH [MH100024, 3, NS36715]
- Greek State Scholarships Foundation
- Johns Hopkins P30 Center for Neuroscience Research [NS050274]
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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.
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