Synaptic localization and activity of ADAM10 regulate excitatory synapses through N-cadherin cleavage
Journal of Neuroscience. 2010-12-01; 30(48): 16343-16355
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1. J Neurosci. 2010 Dec 1;30(48):16343-55. doi: 10.1523/JNEUROSCI.1984-10.2010.
Synaptic localization and activity of ADAM10 regulate excitatory synapses through
Malinverno M(1), Carta M, Epis R, Marcello E, Verpelli C, Cattabeni F, Sala C,
Mulle C, Di Luca M, Gardoni F.
(1)Department of Pharmacological Sciences, University of Milan, 20133 Milan,
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.
PMID: 21123580 [Indexed for MEDLINE]