Regulatory mechanisms of AMPA receptors in synaptic plasticity

被引：696

作者：

Derkach, Victor A. ^{[1
]}

Oh, Michael C. ^{[1
]}

Guire, Eric S. ^{[1
]}

Soderling, Thomas R. ^{[1
]}

机构：

[1] Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97239 USA

来源：

NATURE REVIEWS NEUROSCIENCE | 2007年 / 8卷 / 02期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1038/nrn2055

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Activity-dependent changes in the strength of excitatory synapses are a cellular mechanism for the plasticity of neuronal networks that is widely recognized to underlie cognitive functions such as learning and memory. AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)-type glutamate receptors (AMPARs) are the main transducers of rapid excitatory transmission in the mammalian CNS, and recent discoveries indicate that the mechanisms which regulate AMPARs are more complex than previously thought. This review focuses on recent evidence that alterations to AMPAR functional properties are coupled to their trafficking, cytoskeletal dynamics and local protein synthesis. These relationships offer new insights into the regulation of AMPARs and synaptic strength by cellular signalling.

引用

页码：101 / 113

页数：13

共 181 条

[1] PAK3 mutation in nonsyndromic X-linked mental retardation [J].

Allen, KM ;

Gleeson, JG ;

Bagrodia, S ;

Partington, MW ;

MacMillan, JC ;

Cerione, RA ;

Mulley, JC ;

Walsh, CA .

NATURE GENETICS, 1998, 20 (01) :25-30

[2] Metabotropic glutamate receptors: electrophysiological properties and role in plasticity [J].

Anwyl, R .

BRAIN RESEARCH REVIEWS, 1999, 29 (01) :83-120

[3] Localization of translational components at the ultramicroscopic level at postsynaptic sites of the rat brain [J].

Asaki, C ;

Usuda, N ;

Nakazawa, A ;

Kametani, K ;

Suzuki, T .

BRAIN RESEARCH, 2003, 972 (1-2) :168-176

[4] Removal of AMPA receptors (AMPARs) from synapses is preceded by transient endocytosis of extrasynaptic AMPARs [J].

Ashby, MC ;

De La Rue, SA ;

Ralph, GS ;

Uney, J ;

Collingridge, GL ;

Henley, JM .

JOURNAL OF NEUROSCIENCE, 2004, 24 (22) :5172-5176

[5] Bidirectional regulation of cytoplasmic polyadenylation element-binding protein phosphorylation by Ca2+/calmodulin-dependent protein kinase II and protein phosphatase 1 during hippocampal long-term potentiation [J].

Atkins, CM ;

Davare, MA ;

Oh, MC ;

Derkach, V ;

Soderling, TR .

JOURNAL OF NEUROSCIENCE, 2005, 25 (23) :5604-5610

[6] Cytoplasmic polyadenylation element binding protein-dependent protein synthesis is regulated by calcium/calmodulin-cependent protein kinase II [J].

Atkins, CM ;

Nozaki, N ;

Shigeri, Y ;

Soderling, TR .

JOURNAL OF NEUROSCIENCE, 2004, 24 (22) :5193-5201

[7] Long-term potentiation of exogenous glutamate responses at single dendritic spines [J].

Bagal, AA ;

Kao, JPY ;

Tang, CM ;

Thompson, SM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (40) :14434-14439

[8] Control of GluR1 AMPA receptor function by cAMP-dependent protein kinase [J].

Banke, TG ;

Bowie, D ;

Lee, HK ;

Huganir, RL ;

Schousboe, A ;

Traynelis, SF .

JOURNAL OF NEUROSCIENCE, 2000, 20 (01) :89-102

[9] Identification of the Ca2+/calmodulin-dependent protein kinase II regulatory phosphorylation site in the α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate-type glutamate receptor [J].

Barria, A ;

Derkach, V ;

Soderling, T .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (52) :32727-32730

[10] NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII [J].

Barria, A ;

Malinow, R .

NEURON, 2005, 48 (02) :289-301

← 1 2 3 4 5 6 7 8 9 10 →