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^*

^*Corresponding author for this work

Department of Biology

Research output: Contribution to journal › Journal article › peer-review

270 Citations (Scopus)

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
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
Publication status	Published - Oct 2010

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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). Publisher copyright: {\textcopyright} 2010, Springer Nature America, Inc.",

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AU - Gu, Jiaping

AU - Lee, Chi Wai

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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). Publisher copyright: © 2010, Springer Nature America, Inc.

PY - 2010/10

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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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