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

doi:10.1016/j.neuron.2017.10.029

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

School of Medicine

Research output: Contribution to journal › Article › peer-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 language	English (US)
Pages (from-to)	1084-1098.e7
Journal	Neuron
Volume	96
Issue number	5
DOIs	https://doi.org/10.1016/j.neuron.2017.10.029
State	Published - Dec 6 2017

Keywords

AMPA receptor
Neuropilin-2
Plexin receptor
Sema3F
homeostatic plasticity
semaphorin

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/j.neuron.2017.10.029

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Wang, Q., Chiu, S. L., Koropouli, E., Hong, I., Mitchell, S., Easwaran, T. P., Hamilton, N. R., Gustina, A. S., Zhu, Q., Ginty, D. D., Huganir, R. L., & Kolodkin, A. L. (2017). Neuropilin-2/PlexinA3 Receptors Associate with GluA1 and Mediate Sema3F-Dependent Homeostatic Scaling in Cortical Neurons. Neuron, 96(5), 1084-1098.e7. https://doi.org/10.1016/j.neuron.2017.10.029

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

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.",

keywords = "AMPA receptor, Neuropilin-2, Plexin receptor, Sema3F, homeostatic plasticity, semaphorin",

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

note = "Funding Information: We thank Graham Diering, Paul Worley, and Kolodkin laboratory members for helpful discussions and comments on the manuscript. We thank Dontais Johnson for excellent technical assistance, and Kolodkin laboratory members for helpful discussions and assistance. This work was supported by NIH grants MH100024 (Project #3) to A.L.K. and NS36715 to R.L.H., the Greek State Scholarships Foundation to E.K., and The Johns Hopkins P30 Center for Neuroscience Research (NS050274). A.L.K and D.D.G. are investigators of the Howard Hughes Medical Institute. Publisher Copyright: {\textcopyright} 2017 Elsevier Inc.",

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month = dec,

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doi = "10.1016/j.neuron.2017.10.029",

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T1 - Neuropilin-2/PlexinA3 Receptors Associate with GluA1 and Mediate Sema3F-Dependent Homeostatic Scaling in Cortical Neurons

AU - Wang, Qiang

AU - Chiu, Shu Ling

AU - Koropouli, Eleftheria

AU - Hong, Ingie

AU - Mitchell, Sarah

AU - Easwaran, Teresa P.

AU - Hamilton, Natalie R.

AU - Gustina, Ahleah S.

AU - Zhu, Qianwen

AU - Ginty, David D.

AU - Huganir, Richard L.

AU - Kolodkin, Alex L.

N1 - Funding Information: We thank Graham Diering, Paul Worley, and Kolodkin laboratory members for helpful discussions and comments on the manuscript. We thank Dontais Johnson for excellent technical assistance, and Kolodkin laboratory members for helpful discussions and assistance. This work was supported by NIH grants MH100024 (Project #3) to A.L.K. and NS36715 to R.L.H., the Greek State Scholarships Foundation to E.K., and The Johns Hopkins P30 Center for Neuroscience Research (NS050274). A.L.K and D.D.G. are investigators of the Howard Hughes Medical Institute. Publisher Copyright: © 2017 Elsevier Inc.

PY - 2017/12/6

Y1 - 2017/12/6

N2 - 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.

AB - 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.

KW - AMPA receptor

KW - Neuropilin-2

KW - Plexin receptor

KW - Sema3F

KW - homeostatic plasticity

KW - semaphorin

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VL - 96

SP - 1084-1098.e7

JO - Neuron

JF - Neuron

SN - 0896-6273

IS - 5

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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