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@ARTICLE{Grabrucker:164199,
      author       = {Grabrucker, Stefanie and Pagano, Jessica and Schweizer,
                      Johanna and Urrutia-Ruiz, Carolina and Schön, Michael and
                      Thome, Kevin and Ehret, Günter and Grabrucker, Andreas M
                      and Zhang, Rong and Hengerer, Bastian and Bockmann, Jürgen
                      and Verpelli, Chiara and Sala, Carlo and Böckers, Tobias},
      title        = {{A}ctivation of the medial preoptic area ({MPOA})
                      ameliorates loss of maternal behavior in a {S}hank2 mouse
                      model for autism.},
      journal      = {The EMBO journal},
      volume       = {40},
      number       = {5},
      issn         = {0261-4189},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DZNE-2022-00855},
      pages        = {e104267},
      year         = {2021},
      abstract     = {Impairments in social relationships and awareness are
                      features observed in autism spectrum disorders (ASDs).
                      However, the underlying mechanisms remain poorly understood.
                      Shank2 is a high-confidence ASD candidate gene and localizes
                      primarily to postsynaptic densities (PSDs) of excitatory
                      synapses in the central nervous system (CNS). We show here
                      that loss of Shank2 in mice leads to a lack of social
                      attachment and bonding behavior towards pubs independent of
                      hormonal, cognitive, or sensitive deficits. Shank2-/- mice
                      display functional changes in nuclei of the social
                      attachment circuit that were most prominent in the medial
                      preoptic area (MPOA) of the hypothalamus. Selective
                      enhancement of MPOA activity by DREADD technology
                      re-established social bonding behavior in Shank2-/- mice,
                      providing evidence that the identified circuit might be
                      crucial for explaining how social deficits in ASD can
                      arise.},
      keywords     = {Animals / Autistic Disorder: drug therapy / Autistic
                      Disorder: etiology / Autistic Disorder: metabolism /
                      Autistic Disorder: pathology / Disease Models, Animal /
                      Female / Interpersonal Relations / Male / Maternal Behavior:
                      drug effects / Mice / Mice, Inbred C57BL / Mice, Knockout /
                      Nerve Tissue Proteins: physiology / Piperazines:
                      pharmacology / Preoptic Area: drug effects / Preoptic Area:
                      metabolism / Preoptic Area: pathology / Synapses / SHANK3
                      (Other) / autism spectrum disorders (Other) / bonding
                      (Other) / social behavior (Other) / synapse (Other) / DREADD
                      agonist compound 21 (NLM Chemicals) / Nerve Tissue Proteins
                      (NLM Chemicals) / Piperazines (NLM Chemicals) / Shank2
                      protein, mouse (NLM Chemicals)},
      cin          = {AG Böckers},
      ddc          = {570},
      cid          = {I:(DE-2719)1910002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33491217},
      pmc          = {pmc:PMC7917557},
      doi          = {10.15252/embj.2019104267},
      url          = {https://pub.dzne.de/record/164199},
}