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PMID:11754835

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Citation

Grunwald, IC, Korte, M, Wolfer, D, Wilkinson, GA, Unsicker, K, Lipp, HP, Bonhoeffer, T and Klein, R (2001) Kinase-independent requirement of EphB2 receptors in hippocampal synaptic plasticity. Neuron 32:1027-40

Abstract

During development, Eph receptors mediate the repulsive axon guidance function of ephrins, a family of membrane attached ligands with their own receptor-like signaling potential. In cultured glutamatergic neurons, EphB2 receptors were recently shown to associate with NMDA receptors at synaptic sites and were suggested to play a role in synaptogenesis. Here we show that Eph receptor stimulation in cultured neurons modulates signaling pathways implicated in synaptic plasticity, suggesting cross-talk with NMDA receptor-activated pathways. Mice lacking EphB2 have normal hippocampal synapse morphology, but display defects in synaptic plasticity. In EphB2(-/-) hippocampal slices, protein synthesis-dependent long-term potentiation (LTP) was impaired, and two forms of synaptic depression were completely extinguished. Interestingly, targeted expression of a carboxy-terminally truncated form of EphB2 rescued the EphB2 null phenotype, indicating that EphB2 kinase signaling is not required for these EphB2-mediated functions.

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PubMed

Keywords

Age Factors; Animals; Behavior, Animal/physiology; Electrophysiology; Ephrin-B1; Ephrin-B3; Gene Expression/physiology; Hippocampus/cytology; Hippocampus/physiology; Lac Operon; Ligands; Long-Term Potentiation/physiology; Membrane Proteins/genetics; Membrane Proteins/metabolism; Mice; Mice, Knockout; Neural Inhibition/physiology; Neuronal Plasticity/physiology; Neurons/cytology; Neurons/enzymology; Protein Kinases/metabolism; RNA, Messenger/analysis; Receptor Protein-Tyrosine Kinases/genetics; Receptor Protein-Tyrosine Kinases/metabolism; Receptor, EphB2; Receptors, N-Methyl-D-Aspartate/metabolism; Signal Transduction/physiology; Synapses/physiology; beta-Galactosidase/genetics

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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