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@ARTICLE{Kambali:276799,
      author       = {Kambali, Maltesh and Li, Yan and Unichenko, Petr and Feria
                      Pliego, Jessica A and Yadav, Rachita and Liu, Jing and
                      McGuinness, Patrick and Cobb, Johanna G and Wang, Muxiao and
                      Nagarajan, Rajasekar and Lyu, Jinrui and Vongsouthi, Vanessa
                      and Jackson, Colin J and Engin, Elif and Coyle, Joseph T and
                      Shin, Jaeweon and Hodgson, Nathaniel W and Hensch, Takao K
                      and Talkowski, Michael E and Homanics, Gregg E and
                      Bolshakov, Vadim Y and Henneberger, Christian and Rudolph,
                      Uwe},
      title        = {{A}n increased copy number of glycine decarboxylase
                      ({GLDC}) associated with psychosis reduces extracellular
                      glycine and impairs {NMDA} receptor function.},
      journal      = {Molecular psychiatry},
      volume       = {30},
      number       = {3},
      issn         = {1359-4184},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2025-00324},
      pages        = {927 - 942},
      year         = {2025},
      abstract     = {Glycine is an obligatory co-agonist at excitatory NMDA
                      receptors in the brain, especially in the dentate gyrus,
                      which has been postulated to be crucial for the development
                      of psychotic associations and memories with psychotic
                      content. Drugs modulating glycine levels are in clinical
                      development for improving cognition in schizophrenia.
                      However, the functional relevance of the regulation of
                      glycine metabolism by endogenous enzymes is unclear. Using a
                      chromosome-engineered allelic series in mice, we report that
                      a triplication of the gene encoding the glycine-catabolizing
                      enzyme glycine decarboxylase (GLDC) - as found on a small
                      supernumerary marker chromosome in patients with psychosis -
                      reduces extracellular glycine levels as determined by
                      optical fluorescence resonance energy transfer (FRET) in
                      dentate gyrus (DG) and suppresses long-term potentiation
                      (LTP) in mPP-DG synapses but not in CA3-CA1 synapses,
                      reduces the activity of biochemical pathways implicated in
                      schizophrenia and mitochondrial bioenergetics, and displays
                      deficits in schizophrenia-like behaviors which are in part
                      known to be dependent on the activity of the dentate gyrus,
                      e.g., prepulse inhibition, startle habituation, latent
                      inhibition, working memory, sociability and social
                      preference. Our results demonstrate that Gldc negatively
                      regulates long-term synaptic plasticity in the dentate gyrus
                      in mice, suggesting that an increase in GLDC copy number
                      possibly contributes to the development of psychosis in
                      humans.},
      keywords     = {Animals / Glycine Dehydrogenase (Decarboxylating):
                      metabolism / Glycine Dehydrogenase (Decarboxylating):
                      genetics / Mice / Glycine: metabolism / Receptors,
                      N-Methyl-D-Aspartate: metabolism / Receptors,
                      N-Methyl-D-Aspartate: genetics / Dentate Gyrus: metabolism /
                      Long-Term Potentiation: genetics / Psychotic Disorders:
                      metabolism / Psychotic Disorders: genetics / Male /
                      Schizophrenia: metabolism / Schizophrenia: genetics / Humans
                      / Mice, Inbred C57BL / Synapses: metabolism / Neuronal
                      Plasticity: physiology / Glycine Dehydrogenase
                      (Decarboxylating) (NLM Chemicals) / Glycine (NLM Chemicals)
                      / Receptors, N-Methyl-D-Aspartate (NLM Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {610},
      cid          = {I:(DE-2719)1013029},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39210012},
      doi          = {10.1038/s41380-024-02711-5},
      url          = {https://pub.dzne.de/record/276799},
}