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@ARTICLE{Lu:1020020,
      author       = {Lu, Han and Diaz, Sandra and Lenz, Maximilian and Vlachos,
                      Andreas},
      title        = {{I}nterplay between homeostatic synaptic scaling and
                      homeostatic structural plasticity maintains the robust
                      firing rate of neural networks},
      journal      = {eLife},
      volume       = {12},
      reportid     = {FZJ-2023-05835},
      pages        = {RP88376},
      year         = {2025},
      abstract     = {Critical network states and neural plasticity are essential
                      for flexible behavior in an ever-changing environment, which
                      allows for efficient information processing and
                      experience-based learning. Synaptic-weight-based Hebbian
                      plasticity and homeostatic synaptic scaling were considered
                      the key players in enabling memory while stabilizing network
                      dynamics. However, spine-number-based structural plasticity
                      is not consistently reported as a homeostatic mechanism,
                      leading to an insufficient under-standing of its functional
                      impact. Here, we combined live-cell microscopy of
                      eGPF-tagged neurons in organotypic entorhinal-hippocampal
                      tissue cultures and computational modeling to study the
                      re-sponse of structural plasticity under activity
                      perturbations and its interplay with homeostatic synaptic
                      scaling. By following individual dendritic segments, we
                      demonstrated that the inhibition of excitatory
                      neurotransmission did not linearly regulate dendritic spine
                      density: Inhibition of AMPA receptors with a low
                      concentration of
                      2,3-dioxo-6-nitro-7-sulfamoyl-benzo[f]quinoxaline (NBQX, 200
                      nM) sig-nificantly increased the spine density while
                      complete blockade of AMPA receptors with 50 µM NBQX reduced
                      spine density. Motivated by these results, we established
                      network simulations in which a biphasic structural
                      plasticity rule governs the activity-dependent formation of
                      synapses. We showed that this bi-phasic rule maintained
                      neural activity homeostasis upon stimulation and permitted
                      both synapse formation and synapse loss, depending on the
                      degree of activity deprivation. Homeostatic synaptic scaling
                      affected the recurrent connectivity, modulated the network
                      activity, and influenced the outcome of structural
                      plasticity. It reduced stimulation-triggered homeostatic
                      synapse loss by downscaling synaptic weights; meanwhile, it
                      rescued silencing-induced synapse degeneration by
                      am-plifying recurrent inputs via upscaling to reactivate
                      silent neurons. Their interplay explains divergent results
                      obtained in varied experimental settings. In summary,
                      calcium-based synaptic scaling and homeostatic structural
                      plasticity rules compete and compensate one another other to
                      achieve an eco-nomical and robust control of firing rate
                      homeostasis.},
      cin          = {JSC},
      cid          = {I:(DE-Juel1)JSC-20090406},
      pnm          = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
                      (SDLs) and Research Groups (POF4-511) / HBP SGA3 - Human
                      Brain Project Specific Grant Agreement 3 (945539) / DFG
                      project G:(GEPRIS)491111487 - Open-Access-Publikationskosten
                      / 2025 - 2027 / Forschungszentrum Jülich (OAPKFZJ)
                      (491111487) / SLNS - SimLab Neuroscience (Helmholtz-SLNS) /
                      ICEI - Interactive Computing E-Infrastructure for the Human
                      Brain Project (800858)},
      pid          = {G:(DE-HGF)POF4-5111 / G:(EU-Grant)945539 /
                      G:(GEPRIS)491111487 / G:(DE-Juel1)Helmholtz-SLNS /
                      G:(EU-Grant)800858},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.7554/eLife.88376.1},
      url          = {https://juser.fz-juelich.de/record/1020020},
}