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@ARTICLE{UrrutiaRuiz:164671,
      author       = {Urrutia-Ruiz, Carolina and Rombach, Daniel and Cursano,
                      Silvia and Gerlach-Arbeiter, Susanne and Schoen, Michael and
                      Bockmann, Juergen and Demestre, Maria and Böckers, Tobias},
      title        = {{D}eletion of the {A}utism-{A}ssociated {P}rotein {SHANK}3
                      {A}bolishes {S}tructural {S}ynaptic {P}lasticity after
                      {B}rain {T}rauma},
      journal      = {International journal of molecular sciences},
      volume       = {23},
      number       = {11},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DZNE-2022-01201},
      pages        = {6081},
      year         = {2022},
      note         = {(CC BY)},
      abstract     = {Autism spectrum disorders (ASDs) are characterized by
                      repetitive behaviors and impairments of sociability and
                      communication. About $1\%$ of ASD cases are caused by
                      mutations of SHANK3, a major scaffolding protein of the
                      postsynaptic density. We studied the role of SHANK3 in
                      plastic changes of excitatory synapses within the central
                      nervous system by employing mild traumatic brain injury
                      (mTBI) in WT and Shank3 knockout mice. In WT mice, mTBI
                      triggered ipsi- and contralateral loss of hippocampal
                      dendritic spines and excitatory synapses with a partial
                      recovery over time. In contrast, no significant synaptic
                      alterations were detected in Shank3∆11−/− mice, which
                      showed fewer dendritic spines and excitatory synapses at
                      baseline. In line, mTBI induced the upregulation of synaptic
                      plasticity-related proteins Arc and p-cofilin only in WT
                      mice. Interestingly, microglia proliferation was observed in
                      WT mice after mTBI but not in Shank3∆11−/− mice.
                      Finally, we detected TBI-induced increased fear memory at
                      the behavioral level, whereas in Shank3∆11−/− animals,
                      the already-enhanced fear memory levels increased only
                      slightly after mTBI. Our data show the lack of structural
                      synaptic plasticity in Shank3 knockout mice that might
                      explain at least in part the rigidity of behaviors, problems
                      in adjusting to new situations and cognitive deficits seen
                      in ASDs. View Full-Text},
      keywords     = {Animals / Autistic Disorder: genetics / Autistic Disorder:
                      metabolism / Brain Injuries, Traumatic: metabolism / Mice /
                      Mice, Knockout / Microfilament Proteins: genetics /
                      Microfilament Proteins: metabolism / Nerve Tissue Proteins:
                      genetics / Nerve Tissue Proteins: metabolism / Neuronal
                      Plasticity: genetics / Synapses: metabolism},
      cin          = {AG Böckers},
      ddc          = {540},
      cid          = {I:(DE-2719)1910002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9181590},
      pubmed       = {pmid:35682760},
      doi          = {10.3390/ijms23116081},
      url          = {https://pub.dzne.de/record/164671},
}