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. 2013 Dec 3;7:244. doi: 10.3389/fncel.2013.00244

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Copyright © 2013 Lazarevic, Pothula, Andres-Alonso and Fejtova.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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(A)Scheme of a presynaptic bouton containing synaptic vesicles that can be assigned to functionally different pools (RRP, RP, RtP), the release machinery (depicted as cytomatrix at the active zone, CAZ) and the presynaptic Ca²⁺ channels Cavs. (B) Prolonged activity deprivation induces extensive structural (enlargement of active zones) and functional (increased RRP and Pr) remodeling of presynaptic active zones, which is associated with a molecular reorganization of the release machinery. Protein synthesis (1) as well as protein degradation via the ubiquitin-proteasome system (UPS), (2) play a role in this process. (C) Depolarization-induced presynaptic muting is characterized by decreased size of RRP, depressed Pr and the reduction of CAZ proteins RIM and Munc13, probably due to their degradation by UPS. Induction/recovery from presynaptic muting also involves regulation of adenylate cyclase activity, which is an upstream regulator of PKA.