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AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression.

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AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression. / Scholz, Ralf; Berberich, Sven; Rathgeber, Louisa; Kolleker, Alexander; Köhr, Georg; Kornau, Hans-Christian.

In: NEURON, Vol. 66, No. 5, 5, 2010, p. 768-780.

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

Harvard

Scholz, R, Berberich, S, Rathgeber, L, Kolleker, A, Köhr, G & Kornau, H-C 2010, 'AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression.', NEURON, vol. 66, no. 5, 5, pp. 768-780. <http://www.ncbi.nlm.nih.gov/pubmed/20547133?dopt=Citation>

APA

Scholz, R., Berberich, S., Rathgeber, L., Kolleker, A., Köhr, G., & Kornau, H-C. (2010). AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression. NEURON, 66(5), 768-780. [5]. http://www.ncbi.nlm.nih.gov/pubmed/20547133?dopt=Citation

Vancouver

Scholz R, Berberich S, Rathgeber L, Kolleker A, Köhr G, Kornau H-C. AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression. NEURON. 2010;66(5):768-780. 5.

Bibtex

@article{9003468cbf2f401581d36f3832ef0dd3,
title = "AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression.",
abstract = "Central nervous system synapses undergo activity-dependent alterations to support learning and memory. Long-term depression (LTD) reflects a sustained reduction of the synaptic AMPA receptor content based on targeted clathrin-mediated endocytosis. Here we report a current-independent form of AMPA receptor signaling, fundamental for LTD. We found that AMPA receptors directly interact via the GluA2 subunit with the synaptic protein BRAG2, which functions as a guanine-nucleotide exchange factor (GEF) for the coat-recruitment GTPase Arf6. BRAG2-mediated catalysis, controlled by ligand-binding and tyrosine phosphorylation of GluA2, activates Arf6 to internalize synaptic AMPA receptors upon LTD induction. Furthermore, acute blockade of the GluA2-BRAG2 interaction and targeted deletion of BRAG2 in mature hippocampal CA1 pyramidal neurons prevents LTD in CA3-to-CA1 cell synapses, irrespective of the induction pathway. We conclude that BRAG2-mediated Arf6 activation triggered by AMPA receptors is the convergent step of different forms of LTD, thus providing an essential mechanism for the control of vesicle formation by endocytic cargo.",
author = "Ralf Scholz and Sven Berberich and Louisa Rathgeber and Alexander Kolleker and Georg K{\"o}hr and Hans-Christian Kornau",
year = "2010",
language = "Deutsch",
volume = "66",
pages = "768--780",
journal = "NEURON",
issn = "0896-6273",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression.

AU - Scholz, Ralf

AU - Berberich, Sven

AU - Rathgeber, Louisa

AU - Kolleker, Alexander

AU - Köhr, Georg

AU - Kornau, Hans-Christian

PY - 2010

Y1 - 2010

N2 - Central nervous system synapses undergo activity-dependent alterations to support learning and memory. Long-term depression (LTD) reflects a sustained reduction of the synaptic AMPA receptor content based on targeted clathrin-mediated endocytosis. Here we report a current-independent form of AMPA receptor signaling, fundamental for LTD. We found that AMPA receptors directly interact via the GluA2 subunit with the synaptic protein BRAG2, which functions as a guanine-nucleotide exchange factor (GEF) for the coat-recruitment GTPase Arf6. BRAG2-mediated catalysis, controlled by ligand-binding and tyrosine phosphorylation of GluA2, activates Arf6 to internalize synaptic AMPA receptors upon LTD induction. Furthermore, acute blockade of the GluA2-BRAG2 interaction and targeted deletion of BRAG2 in mature hippocampal CA1 pyramidal neurons prevents LTD in CA3-to-CA1 cell synapses, irrespective of the induction pathway. We conclude that BRAG2-mediated Arf6 activation triggered by AMPA receptors is the convergent step of different forms of LTD, thus providing an essential mechanism for the control of vesicle formation by endocytic cargo.

AB - Central nervous system synapses undergo activity-dependent alterations to support learning and memory. Long-term depression (LTD) reflects a sustained reduction of the synaptic AMPA receptor content based on targeted clathrin-mediated endocytosis. Here we report a current-independent form of AMPA receptor signaling, fundamental for LTD. We found that AMPA receptors directly interact via the GluA2 subunit with the synaptic protein BRAG2, which functions as a guanine-nucleotide exchange factor (GEF) for the coat-recruitment GTPase Arf6. BRAG2-mediated catalysis, controlled by ligand-binding and tyrosine phosphorylation of GluA2, activates Arf6 to internalize synaptic AMPA receptors upon LTD induction. Furthermore, acute blockade of the GluA2-BRAG2 interaction and targeted deletion of BRAG2 in mature hippocampal CA1 pyramidal neurons prevents LTD in CA3-to-CA1 cell synapses, irrespective of the induction pathway. We conclude that BRAG2-mediated Arf6 activation triggered by AMPA receptors is the convergent step of different forms of LTD, thus providing an essential mechanism for the control of vesicle formation by endocytic cargo.

M3 - SCORING: Zeitschriftenaufsatz

VL - 66

SP - 768

EP - 780

JO - NEURON

JF - NEURON

SN - 0896-6273

IS - 5

M1 - 5

ER -