| First Author | Malinverno M | Year | 2010 |
| Journal | J Neurosci | Volume | 30 |
| Issue | 48 | Pages | 16343-55 |
| PubMed ID | 21123580 | Mgi Jnum | J:263409 |
| Mgi Id | MGI:6189345 | Doi | 10.1523/JNEUROSCI.1984-10.2010 |
| Citation | Malinverno M, et al. (2010) Synaptic localization and activity of ADAM10 regulate excitatory synapses through N-cadherin cleavage. J Neurosci 30(48):16343-55 |
| abstractText | N-Cadherin has an important role during dendrite arborization, axon guidance, and synaptogenesis. In particular, at synaptic sites, N-cadherin is involved in the regulation of cell-cell adhesion and in morphology and plasticity control. Recent studies have shown that N-cadherin can be cleaved by the metalloproteinase ADAM10. Here we demonstrate that impairing ADAM10 localization and activity at synaptic sites decreases its processing of N-cadherin. This leads to an accumulation of the full-length form of N-cadherin, to an increase in spine head width, and to modifications of the number and function of glutamate receptors of AMPA type, both in vitro and in vivo. Our results indicate a key role for ADAM10 in the complex sequence of events through which N-cadherin affects spine maturation and controls structure and function of glutamatergic synapses. |
