The postsynaptic density of excitatory synapses is a huge protein complex, with an estimated molecular weight of about 1 GDa1,2. It is composed of neurotransmitter receptors, scaffold and signaling proteins and is localized at the tip of dendritic spines. In contrast to the presynaptic cytomatrix of the active zone, which is transported to axons in a preassembled form, assembly of the PSD may occur locally concomitant with the maturation of the spine, possibly from filopodial precursors3. This process requires the coordination of several cellular processes, including reorganization of the local actin cytoskeleton, regulated interaction between PSD molecules, transport of membrane proteins into dendrites, and possibly also local synthesis of some components from dendritically localized

*Institut f├╝r Humangenetik, Universit├Ątsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany; [email protected]

mRNAs. In addition, recent evidence shows that selected postsynaptic proteins undergo regulated degradation by the ubiquitin proteasome system4. I discuss here the contributions of these mechanisms to synaptogenesis, as well as their pathological relevance, as discovered in inherited forms of MRs.

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