| First Author | Murai KK | Year | 2002 |
| Journal | Curr Biol | Volume | 12 |
| Issue | 3 | Pages | 181-90 |
| PubMed ID | 11839269 | Mgi Jnum | J:74653 |
| Mgi Id | MGI:2158912 | Doi | 10.1016/s0960-9822(02)00680-2 |
| Citation | Murai KK, et al. (2002) Contactin supports synaptic plasticity associated with hippocampal long-term depression but not potentiation. Curr Biol 12(3):181-90 |
| abstractText | BACKGROUND: Changes in synaptic efficacy are believed to mediate the processes of learning and memory formation. Accumulating evidence implicates cell adhesion molecules in activity-dependent synaptic modifications associated with long-term potentiation (LTP); however, there is no precedence for the selective role of this molecule class in long-term depression (LTD). The mechanisms that modulate these processes still remain unclear. RESULTS: We report a novel role for glycosylphosphatidyl inositol (GPI)-anchored contactin in hippocampal CA1 synaptic plasticity. Contactin selectively supports paired-pulse facilitation (PPF) and NMDA (N-methyl-D-aspartate) receptor-dependent LTD but is not required for synaptic morphology, basal transmission, or LTP. Molecular analyses indicate that contactin is essential for the membrane and synaptic targeting of the contactin-associated protein (Caspr/paranodin) and for the proper distribution of a presumptive ligand, receptor protein tyrosine phosphatase beta (RPTPbeta)/phosphacan. CONCLUSIONS: These results indicate that contactin plays a selective role in synaptic plasticity and identify PPF and LTD, but not LTP, as contactin-dependent processes. Engagement of the contactin-Caspr complex with RPTPbeta may thus regulate cell-cell interactions contributing to specific synaptic plasticity forms. |
