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Neuron-glia communication via EphA4/ephrin-A3 modulates LTP through glial glutamate transport
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2009 (English)In: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, Vol. 12, no 10, 1285-1292 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2009. Vol. 12, no 10, 1285-1292 p.
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Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-127513DOI: 10.1038/nn.2394ISI: 000270170200017OAI: oai:DiVA.org:uu-127513DiVA: diva2:330509
Available from: 2010-07-15 Created: 2010-07-13 Last updated: 2017-12-12Bibliographically approved

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Kullander, Klas

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