synaptic scaling
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2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Giacomo Rapisardi ◽  
Ivan Kryven ◽  
Alex Arenas

AbstractPercolation is a process that impairs network connectedness by deactivating links or nodes. This process features a phase transition that resembles paradigmatic critical transitions in epidemic spreading, biological networks, traffic and transportation systems. Some biological systems, such as networks of neural cells, actively respond to percolation-like damage, which enables these structures to maintain their function after degradation and aging. Here we study percolation in networks that actively respond to link damage by adopting a mechanism resembling synaptic scaling in neurons. We explain critical transitions in such active networks and show that these structures are more resilient to damage as they are able to maintain a stronger connectedness and ability to spread information. Moreover, we uncover the role of local rescaling strategies in biological networks and indicate a possibility of designing smart infrastructures with improved robustness to perturbations.


PLoS Biology ◽  
2021 ◽  
Vol 19 (11) ◽  
pp. e3001448
Author(s):  
Ana Luisa Carvalho ◽  
Dominique Fernandes

2021 ◽  
Author(s):  
Gina G Turrigiano ◽  
Chi-Hong Wu ◽  
Vedakumar Tatavarty ◽  
Pierre M Jean-Beltran ◽  
Andrea Guerrero ◽  
...  

Homeostatic synaptic plasticity requires widespread remodeling of synaptic signaling and scaffolding networks, but the role of posttranslational modifications in this process has not been systematically studied. Using deepscale, quantitative analysis of the phosphoproteome in mouse neocortical neurons, we found wide-spread and temporally complex changes during synaptic scaling up and down. We observed 424 bidirectionally modulated phosphosites that were strongly enriched for synapse-associated proteins, including S1539 in the ASD-associated synaptic scaffold protein Shank3. Using a parallel proteomic analysis performed on Shank3 isolated from rat neocortical neurons by immunoaffinity, we identified two sites that were hypo-phosphorylated during scaling up and hyper-phosphorylated during scaling down: one (rat S1615) that corresponded to S1539 in mouse, and a second highly conserved site, rat S1586. The phosphorylation status of these sites modified the synaptic localization of Shank3 during scaling protocols, and dephosphorylation of these sites via PP2A activity was essential for the maintenance of synaptic scaling up. Finally, phosphomimetic mutations at these sites prevented scaling up but not down, while phosphodeficient mutations prevented scaling down but not up. Thus, an activity-dependent switch between hypo- and hyperphosphorylation at S1586/ S1615 of Shank3 enables scaling up or down, respectively. Collectively our data show that activity-dependent phosphoproteome dynamics are important for the functional reconfiguration of synaptic scaffolds, and can bias synapses toward upward or downward homeostatic plasticity.


EMBO Reports ◽  
2021 ◽  
Author(s):  
David Colameo ◽  
Marek Rajman ◽  
Michael Soutschek ◽  
Silvia Bicker ◽  
Lukas Ziegler ◽  
...  

Cell Reports ◽  
2021 ◽  
Vol 36 (7) ◽  
pp. 109515
Author(s):  
Zikai Zhou ◽  
Guiqin He ◽  
Xiaoyun Zhang ◽  
Xin Lv ◽  
Xiaolin Zhang ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Saeed Aljaberi ◽  
Timothy O'Leary ◽  
Fulvio Forni

2021 ◽  
Author(s):  
Wei Wen ◽  
Gina Turrigiano

Homeostatic plasticity maintains network stability by adjusting excitation, inhibition, or the intrinsic excitability of neurons, but the developmental regulation and coordination of these distinct forms of homeostatic plasticity remains poorly understood. A major contributor to this information gap is the lack of a uniform paradigm for chronically manipulating activity at different developmental stages. To overcome this limitation, we utilized Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to directly suppress neuronal activity in layer (L) 2/3 of mouse primary visual cortex (V1) at two important developmental timepoints: the classic visual system critical period (CP, P24-29), and adulthood (P45-55). We show that 24 hours of DREADD-mediated activity suppression simultaneously induces excitatory synaptic scaling up and intrinsic homeostatic plasticity in L2/3 pyramidal neurons during the CP, consistent with previous observations using prolonged visual deprivation. Importantly, manipulations known to block these forms of homeostatic plasticity when induced pharmacologically or via visual deprivation also prevented DREADD-induced homeostatic plasticity. We next used the same paradigm to suppress activity in adult animals. Surprisingly, while excitatory synaptic scaling persisted into adulthood, intrinsic homeostatic plasticity was completely absent. Finally, we found that homeostatic changes in quantal inhibitory input onto L2/3 pyramidal neurons were absent during the CP but present in adults. Thus, the same population of neurons can express distinct sets of homeostatic plasticity mechanisms at different development stages. Our findings suggest that homeostatic forms of plasticity can be recruited in a modular manner according to the evolving needs of a developing neural circuit.


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