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@ARTICLE{Schatz:143930,
      author       = {K. C. Schatz and L. M. Brown and A. R. Barrett and L. C.
                      Roth and V. Grinevich$^*$ and M. J. Paul},
      title        = {{V}iral rescue of magnocellular vasopressin cells in
                      adolescent {B}rattleboro rats ameliorates diabetes
                      insipidus, but not the hypoaroused phenotype.},
      journal      = {Scientific reports},
      volume       = {9},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2019-01488},
      pages        = {8243},
      year         = {2019},
      abstract     = {Dysregulated arousal often accompanies neurodevelopmental
                      disorders such as attention deficit hyperactivity disorder
                      and autism spectrum disorder. Recently, we have found that
                      adolescent homozygous Brattleboro (Hom) rats, which contain
                      a mutation in the arginine vasopressin (AVP) gene, exhibit
                      lower behavioral arousal than their heterozygous (Het)
                      littermates in the open field test. This hypoaroused
                      phenotype could be due to loss of AVP in magnocellular cells
                      that supply AVP to the peripheral circulation and project to
                      limbic structures or parvocellular cells that regulate the
                      stress axis and other central targets. Alternatively,
                      hypoarousal could be a side effect of diabetes insipidus -
                      polydipsia and polyuria seen in Hom rats due to loss of AVP
                      facilitation of water reabsorption in the kidney. We
                      developed a viral-rescue approach to 'cure' magnocellular
                      AVP cells of their Brattleboro mutation. Infusion of a
                      recombinant adeno-associated virus (rAAV) containing a
                      functional Avp gene and promoter (rAAV-AVP) rescued AVP
                      within magnocellular cells and fiber projections of the
                      paraventricular nucleus of the hypothalamus (PVN) of male
                      and female adolescent Hom rats. Furthermore, water intake
                      was markedly reduced, ameliorating the symptoms of diabetes
                      insipidus. In contrast, open field activity was unaffected.
                      These findings indicate that the hyporaoused phenotype of
                      adolescent Hom rats is not due to the loss of AVP function
                      in magnocellular cells or a side effect of diabetes
                      insipidus, but favors the hypothesis that central,
                      parvocellular AVP mechanisms underlie the regulation of
                      arousal during adolescence.},
      cin          = {V078},
      ddc          = {600},
      cid          = {I:(DE-He78)V078-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31160697},
      pmc          = {pmc:PMC6546688},
      doi          = {10.1038/s41598-019-44776-1},
      url          = {https://inrepo02.dkfz.de/record/143930},
}