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@ARTICLE{Manos:903834,
      author       = {Manos, Thanos and Diaz, Sandra and Tass, Peter A.},
      title        = {{L}ong-{T}erm {D}esynchronization by {C}oordinated {R}eset
                      {S}timulation in a {N}eural {N}etwork {M}odel {W}ith
                      {S}ynaptic and {S}tructural {P}lasticity},
      journal      = {Frontiers in physiology},
      volume       = {12},
      issn         = {1664-042X},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2021-05467},
      pages        = {716556},
      year         = {2021},
      abstract     = {Several brain disorders are characterized by abnormal
                      neuronal synchronization. To specifically counteract
                      abnormal neuronal synchrony and, hence, related symptoms,
                      coordinated reset (CR) stimulation was computationally
                      developed. In principle, successive epochs of synchronizing
                      and desynchronizing stimulation may reversibly move neural
                      networks with plastic synapses back and forth between stable
                      regimes with synchronized and desynchronized firing.
                      Computationally derived predictions have been verified in
                      pre-clinical and clinical studies, paving the way for novel
                      therapies. However, as yet, computational models were not
                      able to reproduce the clinically observed increase of
                      desynchronizing effects of regularly administered CR
                      stimulation intermingled by long stimulation-free epochs. We
                      show that this clinically important phenomenon can be
                      computationally reproduced by taking into account structural
                      plasticity (SP), a mechanism that deletes or generates
                      synapses in order to homeostatically adapt the firing rates
                      of neurons to a set point-like target firing rate in the
                      course of days to months. If we assume that CR stimulation
                      favorably reduces the target firing rate of SP, the
                      desynchronizing effects of CR stimulation increase after
                      long stimulation-free epochs, in accordance with clinically
                      observed phenomena. Our study highlights the pivotal role of
                      stimulation- and dosing-induced modulation of homeostatic
                      set points in therapeutic processes.},
      cin          = {JSC},
      ddc          = {610},
      cid          = {I:(DE-Juel1)JSC-20090406},
      pnm          = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
                      (SDLs) and Research Groups (POF4-511) / SLNS - SimLab
                      Neuroscience (Helmholtz-SLNS) / HBP SGA2 - Human Brain
                      Project Specific Grant Agreement 2 (785907) / JL SMHB -
                      Joint Lab Supercomputing and Modeling for the Human Brain
                      (JL SMHB-2021-2027) / Brain-Scale Simulations
                      $(jinb33_20191101)$ / PhD no Grant - Doktorand ohne
                      besondere Förderung (PHD-NO-GRANT-20170405)},
      pid          = {G:(DE-HGF)POF4-5111 / G:(DE-Juel1)Helmholtz-SLNS /
                      G:(EU-Grant)785907 / G:(DE-Juel1)JL SMHB-2021-2027 /
                      $G:(DE-Juel1)jinb33_20191101$ /
                      G:(DE-Juel1)PHD-NO-GRANT-20170405},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34566681},
      UT           = {WOS:000697676800001},
      doi          = {10.3389/fphys.2021.716556},
      url          = {https://juser.fz-juelich.de/record/903834},
}