ADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity

Jiaping Gu; Chi Wai Lee; Yanjie Fan; Daniel Komlos; Xin Tang; Chicheng Sun; Kuai Yu; H. Criss Hartzell; Gong Chen; James R. Bamburg; James Q. Zheng

doi:10.1038/nn.2634

ADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity

Jiaping Gu, Chi Wai Lee, Yanjie Fan, Daniel Komlos, Xin Tang, Chicheng Sun, Kuai Yu, H. Criss Hartzell, Gong Chen, James R. Bamburg, James Q. Zheng

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272 Scopus citations

Abstract

Dendritic spines undergo actin-based growth and shrinkage during synaptic plasticity, in which the actin depolymerizing factor (ADF)/cofilin family of actin-associated proteins are important. Elevated ADF/cofilin activities often lead to reduced spine size and immature spine morphology but can also enhance synaptic potentiation in some cases. Thus, ADF/cofilin may have distinct effects on postsynaptic structure and function. We found that ADF/cofilin-mediated actin dynamics regulated AMPA receptor (AMPAR) trafficking during synaptic potentiation, which was distinct from actin's structural role in spine morphology. Specifically, elevated ADF/cofilin activity markedly enhanced surface addition of AMPARs after chemically induced long-term potentiation (LTP), whereas inhibition of ADF/cofilin abolished AMPAR addition. We found that chemically induced LTP elicited a temporal sequence of ADF/cofilin dephosphorylation and phosphorylation that underlies AMPAR trafficking and spine enlargement. These findings suggest that temporally regulated ADF/cofilin activities function in postsynaptic modifications of receptor number and spine size during synaptic plasticity.

Original language	English (US)
Pages (from-to)	1208-1215
Number of pages	8
Journal	Nature Neuroscience
Volume	13
Issue number	10
DOIs	https://doi.org/10.1038/nn.2634
State	Published - Oct 2010

All Science Journal Classification (ASJC) codes

General Neuroscience

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10.1038/nn.2634

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@article{ca72f50dc37f40e09619dbcd9770c2d4,

title = "ADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity",

abstract = "Dendritic spines undergo actin-based growth and shrinkage during synaptic plasticity, in which the actin depolymerizing factor (ADF)/cofilin family of actin-associated proteins are important. Elevated ADF/cofilin activities often lead to reduced spine size and immature spine morphology but can also enhance synaptic potentiation in some cases. Thus, ADF/cofilin may have distinct effects on postsynaptic structure and function. We found that ADF/cofilin-mediated actin dynamics regulated AMPA receptor (AMPAR) trafficking during synaptic potentiation, which was distinct from actin's structural role in spine morphology. Specifically, elevated ADF/cofilin activity markedly enhanced surface addition of AMPARs after chemically induced long-term potentiation (LTP), whereas inhibition of ADF/cofilin abolished AMPAR addition. We found that chemically induced LTP elicited a temporal sequence of ADF/cofilin dephosphorylation and phosphorylation that underlies AMPAR trafficking and spine enlargement. These findings suggest that temporally regulated ADF/cofilin activities function in postsynaptic modifications of receptor number and spine size during synaptic plasticity.",

author = "Jiaping Gu and Lee, {Chi Wai} and Yanjie Fan and Daniel Komlos and Xin Tang and Chicheng Sun and Kuai Yu and Hartzell, {H. Criss} and Gong Chen and Bamburg, {James R.} and Zheng, {James Q.}",

note = "Funding Information: This research was supported by grants from the US National Institutes of Health to J.Q.Z. (GM083889 GM084363, and HD023315), J.R.B. (NS40371), G.C. (NS054858) and H.C.H. (EY014852 and GM60448).",

year = "2010",

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doi = "10.1038/nn.2634",

language = "English (US)",

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T1 - ADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity

AU - Gu, Jiaping

AU - Lee, Chi Wai

AU - Fan, Yanjie

AU - Komlos, Daniel

AU - Tang, Xin

AU - Sun, Chicheng

AU - Yu, Kuai

AU - Hartzell, H. Criss

AU - Chen, Gong

AU - Bamburg, James R.

AU - Zheng, James Q.

N1 - Funding Information: This research was supported by grants from the US National Institutes of Health to J.Q.Z. (GM083889 GM084363, and HD023315), J.R.B. (NS40371), G.C. (NS054858) and H.C.H. (EY014852 and GM60448).

PY - 2010/10

Y1 - 2010/10

N2 - Dendritic spines undergo actin-based growth and shrinkage during synaptic plasticity, in which the actin depolymerizing factor (ADF)/cofilin family of actin-associated proteins are important. Elevated ADF/cofilin activities often lead to reduced spine size and immature spine morphology but can also enhance synaptic potentiation in some cases. Thus, ADF/cofilin may have distinct effects on postsynaptic structure and function. We found that ADF/cofilin-mediated actin dynamics regulated AMPA receptor (AMPAR) trafficking during synaptic potentiation, which was distinct from actin's structural role in spine morphology. Specifically, elevated ADF/cofilin activity markedly enhanced surface addition of AMPARs after chemically induced long-term potentiation (LTP), whereas inhibition of ADF/cofilin abolished AMPAR addition. We found that chemically induced LTP elicited a temporal sequence of ADF/cofilin dephosphorylation and phosphorylation that underlies AMPAR trafficking and spine enlargement. These findings suggest that temporally regulated ADF/cofilin activities function in postsynaptic modifications of receptor number and spine size during synaptic plasticity.

AB - Dendritic spines undergo actin-based growth and shrinkage during synaptic plasticity, in which the actin depolymerizing factor (ADF)/cofilin family of actin-associated proteins are important. Elevated ADF/cofilin activities often lead to reduced spine size and immature spine morphology but can also enhance synaptic potentiation in some cases. Thus, ADF/cofilin may have distinct effects on postsynaptic structure and function. We found that ADF/cofilin-mediated actin dynamics regulated AMPA receptor (AMPAR) trafficking during synaptic potentiation, which was distinct from actin's structural role in spine morphology. Specifically, elevated ADF/cofilin activity markedly enhanced surface addition of AMPARs after chemically induced long-term potentiation (LTP), whereas inhibition of ADF/cofilin abolished AMPAR addition. We found that chemically induced LTP elicited a temporal sequence of ADF/cofilin dephosphorylation and phosphorylation that underlies AMPAR trafficking and spine enlargement. These findings suggest that temporally regulated ADF/cofilin activities function in postsynaptic modifications of receptor number and spine size during synaptic plasticity.

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ADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity

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