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

TitleADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity
Authors
Issue Date2010
Citation
Nature Neuroscience, 2010, v. 13, n. 10, p. 1208-1215 How to Cite?
AbstractDendritic 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. © 2010 Nature America, Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/219863
ISSN
2015 Impact Factor: 16.724
2015 SCImago Journal Rankings: 13.558

 

DC FieldValueLanguage
dc.contributor.authorGu, Jiaping-
dc.contributor.authorLee, Chi Wai-
dc.contributor.authorFan, Yanjie-
dc.contributor.authorKomlos, Daniel-
dc.contributor.authorTang, Xin-
dc.contributor.authorSun, Chicheng-
dc.contributor.authorYu, Kuai-
dc.contributor.authorHartzell, H. Criss-
dc.contributor.authorChen, Gong-
dc.contributor.authorBamburg, James R.-
dc.contributor.authorZheng, James Q.-
dc.date.accessioned2015-09-24T04:44:09Z-
dc.date.available2015-09-24T04:44:09Z-
dc.date.issued2010-
dc.identifier.citationNature Neuroscience, 2010, v. 13, n. 10, p. 1208-1215-
dc.identifier.issn1097-6256-
dc.identifier.urihttp://hdl.handle.net/10722/219863-
dc.description.abstractDendritic 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. © 2010 Nature America, Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofNature Neuroscience-
dc.titleADF/cofilin-mediated actin dynamics regulate AMPA receptor trafficking during synaptic plasticity-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1038/nn.2634-
dc.identifier.pmid20835250-
dc.identifier.scopuseid_2-s2.0-77957275697-
dc.identifier.volume13-
dc.identifier.issue10-
dc.identifier.spage1208-
dc.identifier.epage1215-

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