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  Neuron-glia communication via EphA4/ephrin-A3 modulates LTP through glial glutamate transport

Filosa, A., Paixao, S., Honsek, S. D., Carmona, M. A., Becker, L., Feddersen, B., et al. (2009). Neuron-glia communication via EphA4/ephrin-A3 modulates LTP through glial glutamate transport. Nature Neuroscience, 12(10), 1285-1292. doi:10.1038/nn.2394.

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Filosa, Alessandro1, Author           
Paixao, Sonia1, Author           
Honsek, S. D.2, Author
Carmona, M. A.2, Author
Becker, L.2, Author
Feddersen, B.2, Author
Gaitanos, Louise1, Author           
Rudhard, Y.2, Author
Schoepfer, R.2, Author
Klopstock, T.2, Author
Kullander, K.2, Author
Rose, C. R.2, Author
Pasquale, E. B.2, Author
Klein, Rüdiger1, Author           
Affiliations:
1Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society, ou_1113546              
2[Honsek, Silke D.; Rose, Christine R.] Univ Dusseldorf, Inst Neurobiol, Dusseldorf, Germany.; [Carmona, Maria A.; Pasquale, Elena B.] Burnham Inst Med Res, La Jolla, CA USA.; [Becker, Lore; Klopstock, Thomas] German Res Ctr Environm Hlth GmbH, German Mouse Clin, Inst Expt Genet, Helmholtz Ctr, Munich, Germany.; [Becker, Lore; Feddersen, Berend; Klopstock, Thomas] Univ Munich, Dept Neurol, Friedrich Baur Inst, D-8000 Munich, Germany.; [Rudhard, York; Schoepfer, Ralf] UCL, Mol Pharmacol Lab, London, England.; [Kullander, Klas] Uppsala Univ, Dept Neurosci, Uppsala, Sweden., ou_persistent22              

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 Abstract: Astrocytes are critical participants in synapse development and function, but their role in synaptic plasticity is unclear. Eph receptors and their ephrin ligands have been suggested to regulate neuron-glia interactions, and EphA4-mediated ephrin reverse signaling is required for synaptic plasticity in the hippocampus. Here we show that long-term potentiation (LTP) at the CA3-CA1 synapse is modulated by EphA4 in the postsynaptic CA1 cell and by ephrin-A3, a ligand of EphA4 that is found in astrocytes. Lack of EphA4 increased the abundance of glial glutamate transporters, and ephrin-A3 modulated transporter currents in astrocytes. Pharmacological inhibition of glial glutamate transporters rescued the LTP defects in EphA4 (Epha4) and ephrin-A3 (Efna3) mutant mice. Transgenic overexpression of ephrin-A3 in astrocytes reduces glutamate transporter levels and produces focal dendritic swellings possibly caused by glutamate excitotoxicity. These results suggest that EphA4/ephrin-A3 signaling is a critical mechanism for astrocytes to regulate synaptic function and plasticity.

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Language(s): eng - English
 Dates: 2009-10
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 437293
ISI: 000270170200017
DOI: 10.1038/nn.2394
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Title: Nature Neuroscience
  Other : Nat. Neurosci.
Source Genre: Journal
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Publ. Info: New York, NY : Nature America Inc.
Pages: - Volume / Issue: 12 (10) Sequence Number: - Start / End Page: 1285 - 1292 Identifier: ISSN: 1097-6256
CoNE: https://pure.mpg.de/cone/journals/resource/954925610931