期刊
JOURNAL OF NEUROSCIENCE
卷 30, 期 48, 页码 16343-16355出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1984-10.2010
关键词
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资金
- European Union [PIAP-GA-2008-217902]
- Fondazione CARIPLO [2009.264]
- Telethon-Italy [GGP09196]
- RSTL-CNR
- Regione Lombardia Project [SAL-50-16983 TERDISMENTAL]
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.
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