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@ARTICLE{Pizzarelli:287457,
      author       = {R. Pizzarelli and D. Pimpinella and C. Jacobs and A.
                      Tartacca and U. Kullolli and H. Monyer$^*$ and C. M.
                      Alberini and M. Griguoli},
      title        = {{I}nsulin-like growth factor 2 ({IGF}-2) rescues social
                      deficits in {NLG}3-/y mouse model of {ASD}s.},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {17},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DKFZ-2024-00249},
      pages        = {1332179},
      year         = {2024},
      abstract     = {Autism spectrum disorders (ASDs) comprise developmental
                      disabilities characterized by impairments of social
                      interaction and repetitive behavior, often associated with
                      cognitive deficits. There is no current treatment that can
                      ameliorate most of the ASDs symptomatology; thus,
                      identifying novel therapies is urgently needed. Here, we
                      used the Neuroligin 3 knockout mouse (NLG3-/y), a model that
                      recapitulates the social deficits reported in ASDs patients,
                      to test the effects of systemic administration of IGF-2, a
                      polypeptide that crosses the blood-brain barrier and acts as
                      a cognitive enhancer. We show that systemic IGF-2 treatment
                      reverses the typical defects in social interaction and
                      social novelty discrimination reflective of ASDs-like
                      phenotypes. This effect was not accompanied by any change in
                      spontaneous glutamatergic synaptic transmission in CA2
                      hippocampal region, a mechanism found to be crucial for
                      social novelty discrimination. However, in both NLG3+/y and
                      NLG3-/y mice IGF-2 increased cell excitability. Although
                      further investigation is needed to clarify the cellular and
                      molecular mechanisms underpinning IGF-2 effect on social
                      behavior, our findings highlight IGF-2 as a potential
                      pharmacological tool for the treatment of social
                      dysfunctions associated with ASDs.},
      keywords     = {ASDs (Other) / IGF-2 (Other) / NLG3 -/y mouse (Other) /
                      hippocampus (Other) / social behavior (Other)},
      cin          = {A230},
      ddc          = {610},
      cid          = {I:(DE-He78)A230-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38298376},
      pmc          = {pmc:PMC10827848},
      doi          = {10.3389/fncel.2023.1332179},
      url          = {https://inrepo02.dkfz.de/record/287457},
}