| First Author | Grunwald IC | Year | 2001 |
| Journal | Neuron | Volume | 32 |
| Issue | 6 | Pages | 1027-40 |
| PubMed ID | 11754835 | Mgi Jnum | J:73508 |
| Mgi Id | MGI:2155580 | Doi | 10.1016/s0896-6273(01)00550-5 |
| Citation | Grunwald IC, et al. (2001) Kinase-Independent Requirement of EphB2 Receptors in Hippocampal Synaptic Plasticity. Neuron 32(6):1027-40 |
| abstractText | 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. |
