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@ARTICLE{Vyas:155437,
      author       = {Vyas, Yukti and Jung, Yewon and Lee, Kevin and Garner,
                      Craig C and Montgomery, Johanna M},
      title        = {{I}n vitro zinc supplementation alters synaptic deficits
                      caused by autism spectrum disorder-associated {S}hank2 point
                      mutations in hippocampal neurons.},
      journal      = {Molecular brain},
      volume       = {14},
      number       = {1},
      issn         = {1756-6606},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DZNE-2021-00643},
      pages        = {95},
      year         = {2021},
      abstract     = {Autism Spectrum Disorders (ASDs) are neurodevelopmental
                      disorders characterised by deficits in social interactions
                      and repetitive behaviours. ASDs have a strong genetic basis
                      with mutations involved in the development and function of
                      neural circuitry. Shank proteins act as master regulators of
                      excitatory glutamatergic synapses, and Shank mutations have
                      been identified in people with ASD. Here, we have
                      investigated the impact of ASD-associated Shank2 single
                      nucleotide variants (SNVs) at the synaptic level, and the
                      potential of in vitro zinc supplementation to prevent
                      synaptic deficits. Dissociated rat hippocampal cultures
                      expressing enhanced green fluorescent protein (EGFP) tagged
                      Shank2-Wildtype (WT), and ASD-associated Shank2 single
                      nucleotide variants (SNVs: S557N, V717F, and L1722P), were
                      cultured in the absence or presence of 10 μM zinc. In
                      comparison to Shank2-WT, ASD-associated Shank2 SNVs induced
                      significant decreases in synaptic density and reduced the
                      frequency of miniature excitatory postsynaptic currents.
                      These structural and functional ASD-associated synaptic
                      deficits were prevented by chronic zinc supplementation and
                      further support zinc supplementation as a therapeutic target
                      in ASD.},
      keywords     = {Animals / Animals, Newborn / Autism Spectrum Disorder:
                      genetics / Autism Spectrum Disorder: pathology / Dietary
                      Supplements / Female / Glutamic Acid: metabolism /
                      Hippocampus: pathology / Male / Nerve Tissue Proteins:
                      genetics / Neurons: drug effects / Neurons: metabolism /
                      Neurons: pathology / Point Mutation: genetics / Rats /
                      Synapses: drug effects / Synapses: pathology / Zinc:
                      pharmacology / Autism (Other) / Glutamatergic synapses
                      (Other) / Shank2 (Other) / Zinc supplementation (Other)},
      cin          = {AG Garner},
      ddc          = {610},
      cid          = {I:(DE-2719)1810001},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34167580},
      pmc          = {pmc:PMC8223320},
      doi          = {10.1186/s13041-021-00809-3},
      url          = {https://pub.dzne.de/record/155437},
}