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DHPG-induced STD was entirely mediated by the activation of mGlu5 receptors because it was abrogated by the mGlu5 receptor antagonist, MPEP [2-methyl-6-(phenylethynyl)pyridine], but not by the mGlu1 receptor antagonist, CPCCOEt [7-(hydroxyimino)cyclopropa[<jats:italic>b<\/jats:italic>]chromen-1<jats:italic>a<\/jats:italic>-carboxylate ethyl ester]. Knowing that ephrin-Bs functionally interact with group-I mGlu receptors (Cal\u00f2 et al., 2005), we examined whether pharmacological activation of ephrin-Bs could affect DHPG-induced STD. We activated ephrin-Bs using their cognate receptor, EphB1, under the form of a preclustered EphB1\/Fc chimera. Addition of clustered EphB1\/Fc alone to the slices induced a small but nondecremental depression of excitatory synaptic transmission, which differed from the depression induced by 10 \u03bc<jats:sc>m<\/jats:sc>DHPG. Surprisingly, EphB1\/Fc-induced synaptic depression was abolished by MPEP (but not by CPCCOEt) suggesting that it required the endogenous activation of mGlu5 receptors. In addition, coapplication of DHPG and EphB1\/Fc, resulted in a large and nondecremental long-term depression. The effect of clustered EphB1\/Fc was specific because it was not mimicked by unclustered EphB1\/Fc or clustered EphA1\/Fc. These findings raise the intriguing possibility that changes in synaptic efficacy mediated by mGlu5 receptors are under the control of the ephrin\/Eph receptor system, and that the neuronal actions of ephrins can be targeted by drugs that attenuate mGlu5 receptor signaling.<\/jats:p>","DOI":"10.1523\/jneurosci.4834-09.2010","type":"journal-article","created":{"date-parts":[[2010,2,24]],"date-time":"2010-02-24T18:28:22Z","timestamp":1267036102000},"page":"2835-2843","source":"Crossref","is-referenced-by-count":15,"title":["Interaction between Ephrins and mGlu5 Metabotropic Glutamate Receptors in the Induction of Long-Term Synaptic Depression in the 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