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@ARTICLE{Chelini:269432,
      author       = {Chelini, Gabriele and Mirzapourdelavar, Hadi and Durning,
                      Peter and Baidoe-Ansah, David and Sethi, Manveen K. and
                      O’Donovan, Sinead M. and Klengel, Torsten and Balasco,
                      Luigi and Berciu, Cristina and Boyer-Boiteau, Anne and
                      McCullumsmith, Robert and Ressler, Kerry J. and Zaia, Joseph
                      and Bozzi, Yuri and Dityatev, Alexander and Berretta,
                      Sabina},
      title        = {{F}ocal clusters of peri-synaptic matrix contribute to
                      activity-dependent plasticity and memory in mice},
      journal      = {Cell reports},
      volume       = {43},
      number       = {5},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-00529},
      pages        = {114112},
      year         = {2024},
      abstract     = {Recent findings show that effective integration of novel
                      information in the brain requires coordinated processes of
                      homo- and heterosynaptic plasticity. In this work, we
                      hypothesize that activity-dependent remodeling of the
                      peri-synaptic extracellular matrix (ECM) contributes to
                      these processes. We show that clusters of the peri-synaptic
                      ECM, recognized by CS56 antibody, emerge in response to
                      sensory stimuli, showing temporal and spatial coincidence
                      with dendritic spine plasticity. Using CS56
                      co-immunoprecipitation of synaptosomal proteins, we identify
                      several molecules involved in Ca2+ signaling, vesicle
                      cycling, and AMPA-receptor exocytosis, thus suggesting a
                      role in long-term potentiation (LTP). Finally, we show that,
                      in the CA1 hippocampal region, the attenuation of CS56
                      glycoepitopes, through the depletion of versican as one of
                      its main carriers, impairs LTP and object location memory in
                      mice. These findings show that activity-dependent remodeling
                      of the peri-synaptic ECM regulates the induction and
                      consolidation of LTP, contributing to hippocampal-dependent
                      memory.},
      keywords     = {Animals / Extracellular Matrix: metabolism / Long-Term
                      Potentiation: physiology / Mice / Neuronal Plasticity:
                      physiology / Memory: physiology / Synapses: metabolism /
                      Synapses: physiology / Mice, Inbred C57BL / Male / CA1
                      Region, Hippocampal: metabolism / CA1 Region, Hippocampal:
                      physiology / CA1 Region, Hippocampal: cytology /
                      Hippocampus: metabolism / Hippocampus: physiology / CP: Cell
                      biology (Other) / CP: Neuroscience (Other) / CS clusters
                      (Other) / chondrotin sulfate proteoglycans (Other) /
                      extracellular matrix (Other) / hippocampus (Other) /
                      immunoprecipitation (Other) / learning and memory (Other) /
                      sensory manipulation (Other) / synaptic plasticity (Other) /
                      versican (Other)},
      cin          = {AG Dityatev},
      ddc          = {610},
      cid          = {I:(DE-2719)1310007},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11251421},
      pubmed       = {pmid:38676925},
      doi          = {10.1016/j.celrep.2024.114112},
      url          = {https://pub.dzne.de/record/269432},
}