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

Neuron | 2017

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.

Pubmed ID: 29154130 RIS Download

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Associated grants

  • Agency: NINDS NIH HHS, United States
    Id: P30 NS050274
  • Agency: NINDS NIH HHS, United States
    Id: R35 NS097344
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS036715
  • Agency: NINDS NIH HHS, United States
    Id: T32 NS091018
  • Agency: NIMH NIH HHS, United States
    Id: P50 MH100024
  • Agency: Howard Hughes Medical Institute, United States

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