Journal
NATURE NEUROSCIENCE
Volume 12, Issue 10, Pages 1285-U106Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2394
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Funding
- Fundacao para a Ciencia e Tecnologia of Portugal
- Programa Operacional Ciencia e Inovacao
- Fundo Social Europeu
- Fundacion Espanola para la Ciencia y la Tecnologia
- European Union
- Deutsche Forschungsgemeinschaft [SPP1172]
- Max-Planck Society
- Wellcome Trust
- Biotechnology and Biological Sciences Research Council, UK
- German National Genome Research Network [01GR0430]
- US National Institutes of Health [HD025938]
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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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