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@ARTICLE{Bertan:154291,
      author       = {Bertan, Fabio and Wischhof, Lena and Sosulina, Liudmila and
                      Mittag, Manuel and Dalügge, Dennis and Fornarelli,
                      Alessandra and Gardoni, Fabrizio and Marcello, Elena and Di
                      Luca, Monica and Fuhrmann, Martin and Remy, Stefan and Bano,
                      Daniele and Nicotera, Pierluigi},
      title        = {{L}oss of {R}yanodine {R}eceptor 2 impairs neuronal
                      activity-dependent remodeling of dendritic spines and
                      triggers compensatory neuronal hyperexcitability.},
      journal      = {Cell death and differentiation},
      volume       = {27},
      number       = {12},
      issn         = {1476-5403},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {DZNE-2021-00145},
      pages        = {3354 - 3373},
      year         = {2020},
      note         = {ISSN 1476-5403 not unique: **3 hits**.},
      abstract     = {Dendritic spines are postsynaptic domains that shape
                      structural and functional properties of neurons. Upon
                      neuronal activity, Ca2+ transients trigger signaling
                      cascades that determine the plastic remodeling of dendritic
                      spines, which modulate learning and memory. Here, we study
                      in mice the role of the intracellular Ca2+ channel Ryanodine
                      Receptor 2 (RyR2) in synaptic plasticity and memory
                      formation. We demonstrate that loss of RyR2 in pyramidal
                      neurons of the hippocampus impairs maintenance and
                      activity-evoked structural plasticity of dendritic spines
                      during memory acquisition. Furthermore, post-developmental
                      deletion of RyR2 causes loss of excitatory synapses,
                      dendritic sparsification, overcompensatory excitability,
                      network hyperactivity and disruption of spatially tuned
                      place cells. Altogether, our data underpin RyR2 as a link
                      between spine remodeling, circuitry dysfunction and memory
                      acquisition, which closely resemble pathological mechanisms
                      observed in neurodegenerative disorders.},
      keywords     = {Animals / Dendritic Spines: physiology / Female /
                      Hippocampus: metabolism / Male / Mice / Mice, Inbred C57BL /
                      Mice, Knockout / Neuronal Plasticity: physiology / Pyramidal
                      Cells: metabolism / Ryanodine Receptor Calcium Release
                      Channel: metabolism / Synapses: physiology},
      cin          = {AG Nicotera / Bano ; AG Bano / AG Remy / AG Fuhrmann},
      ddc          = {610},
      cid          = {I:(DE-2719)1013003 / I:(DE-2719)1013006 /
                      I:(DE-2719)1011004},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32641776},
      pmc          = {pmc:PMC7853040},
      doi          = {10.1038/s41418-020-0584-2},
      url          = {https://pub.dzne.de/record/154291},
}