Journal
EMBO JOURNAL
Volume 30, Issue 3, Pages 569-581Publisher
WILEY
DOI: 10.1038/emboj.2010.336
Keywords
ProSAP2; PSD; Shank3; synapse; zinc
Categories
Funding
- Deutsche Forschungsgemeinschaft [DFG: SFB497-B8, BO 1718, 3-1, SFB 779/B8, /B9]
- Ulm University, International Graduate School Molecular Medicine
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Neuronal morphology and number of synapses is not static, but can change in response to a variety of factors, a process called synaptic plasticity. These structural and molecular changes are believed to represent the basis for learning and memory, thereby underling both the developmental and activity-dependent remodelling of excitatory synapses. Here, we report that Zn2+ ions, which are highly enriched within the postsynaptic density (PSD), are able to influence the recruitment of ProSAP/Shank proteins to PSDs in a family member-specific manner during the course of synaptogenesis and synapse maturation. Through selectively overexpressing each family member at excitatory postsynapses and comparing this to shRNA-mediated knockdown, we could demonstrate that only the overexpression of zinc-sensitive ProSAP1/Shank2 or ProSAP2/Shank3 leads to increased synapse density, although all of them cause a decrease upon knockdown. Furthermore, depletion of synaptic Zn2+ along with the knockdown of zinc-insensitive Shank1 causes the rapid disintegration of PSDs and the loss of several postsynaptic molecules including Homer1, PSD-95 and NMDA receptors. These findings lead to the model that the concerted action of ProSAP/Shank and Zn2+ is essential for the structural integrity of PSDs and moreover that it is an important element of synapse formation, maturation and structural plasticity. The EMBO Journal (2011) 30, 569-581. doi:10.1038/emboj.2010.336; Published online 7 January 2011
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