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@ARTICLE{Schoch:827653,
      author       = {Schoch, Hannah and Kreibich, Arati S. and Ferri, Sarah L.
                      and White, Rachel S. and Bohorquez, Dominique and Banerjee,
                      Anamika and Port, Russell G. and Dow, Holly C. and Cordero,
                      Lucero and Pallathra, Ashley A. and Kim, Hyong and Li,
                      Hongzhe and Bilker, Warren B. and Hirano, Shinji and
                      Schultz, Robert T. and Borgmann-Winter, Karin and Hahn,
                      Chang-Gyu and Feldmeyer, Dirk and Carlson, Gregory C. and
                      Abel, Ted and Brodkin, Edward S.},
      title        = {{S}ociability {D}eficits and {A}ltered {A}mygdala
                      {C}ircuits in {M}ice {L}acking {P}cdh10, an {A}utism
                      {A}ssociated {G}ene},
      journal      = {Biological psychiatry},
      volume       = {81},
      number       = {3},
      issn         = {0006-3223},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2017-01767},
      pages        = {193 - 202},
      year         = {2017},
      abstract     = {BackgroundBehavioral symptoms in individuals with autism
                      spectrum disorder (ASD) have been attributed to abnormal
                      neuronal connectivity, but the molecular bases of these
                      behavioral and brain phenotypes are largely unknown. Human
                      genetic studies have implicated PCDH10, a member of the δ2
                      subfamily of nonclustered protocadherin genes, in ASD.
                      PCDH10 expression is enriched in the basolateral amygdala, a
                      brain region implicated in the social deficits of ASD.
                      Previous reports indicate that Pcdh10 plays a role in axon
                      outgrowth and glutamatergic synapse elimination, but its
                      roles in social behaviors and amygdala neuronal connectivity
                      are unknown. We hypothesized that haploinsufficiency of
                      Pcdh10 would reduce social approach behavior and alter the
                      structure and function of amygdala circuits.MethodsMice
                      lacking one copy of Pcdh10 (Pcdh10+/–) and wild-type
                      littermates were assessed for social approach and other
                      behaviors. The lateral/basolateral amygdala was assessed for
                      dendritic spine number and morphology, and amygdala circuit
                      function was studied using voltage-sensitive dye imaging.
                      Expression of Pcdh10 and N-methyl-D-aspartate receptor
                      (NMDAR) subunits was assessed in postsynaptic density
                      fractions of the amygdala.ResultsMale Pcdh10+/– mice have
                      reduced social approach behavior, as well as impaired gamma
                      synchronization, abnormal spine morphology, and reduced
                      levels of NMDAR subunits in the amygdala. Social approach
                      deficits in Pcdh10+/– male mice were rescued with acute
                      treatment with the NMDAR partial agonist
                      d-cycloserine.ConclusionsOur studies reveal that male
                      Pcdh10+/– mice have synaptic and behavioral deficits, and
                      establish Pcdh10+/– mice as a novel genetic model for
                      investigating neural circuitry and behavioral changes
                      relevant to ASD.},
      cin          = {INM-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {571 - Connectivity and Activity (POF3-571)},
      pid          = {G:(DE-HGF)POF3-571},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000397011700007},
      pubmed       = {pmid:27567313},
      doi          = {10.1016/j.biopsych.2016.06.008},
      url          = {https://juser.fz-juelich.de/record/827653},
}