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@ARTICLE{Bohmbach:283021,
      author       = {Bohmbach, Kirsten and Bauer, Vincent and Henneberger,
                      Christian},
      title        = {{G}lycine and glycine transport control dendritic
                      excitability and spiking.},
      journal      = {Progress in neurobiology},
      volume       = {256},
      issn         = {0301-0082},
      address      = {Jena},
      publisher    = {Elsevier},
      reportid     = {DZNE-2025-01433},
      pages        = {102856},
      year         = {2025},
      abstract     = {Neuronal dendrites integrate excitatory input. They can
                      perform local computations such as coincidence detection by
                      amplifying synchronized local input and dendritic spiking.
                      Extracellular glycine could be a powerful modulator of such
                      processes through its action as a co-agonist at glutamate
                      receptors of the N-methyl-D-aspartate (NMDA) subtype but
                      also as a ligand of inhibitory glycine receptors (GlyRs).
                      Similarly, glycine transporters (GlyTs), an emerging drug
                      target for psychiatric and other diseases, could control
                      dendritic integration through ambient glycine levels. Both
                      hypotheses were tested at dendrites of CA1 pyramidal cells
                      in acute hippocampal slices by pharmacologically analysing
                      how glycine, GlyTs and GlyRs change the postsynaptic
                      response to local dendritic excitatory input. Using
                      microiontophoretic glutamate application, we found that
                      glycine can indeed significantly increase dendritic
                      excitability and dendritic spiking. We also uncovered that
                      GlyTs are powerful modulators of dendritic spiking, which
                      can limit the impact of glycine sources on CA1 pyramidal
                      cells. Our experiments also revealed that GlyRs can have an
                      opposite, inhibitory effect on the slow dendritic spike
                      component. This directly demonstrates that glycine can
                      dynamically enhance dendritic responsiveness to local input
                      and promote dendritic spiking, while GlyTs and GlyRs have an
                      opposing effect. Together, this makes glycinergic signalling
                      a powerful modulator of the nonlinear integration of
                      synaptic input in CA1 radial oblique dendrites.},
      keywords     = {D-serine (Other) / Dendritic excitability (Other) /
                      Dendritic spiking (Other) / Glycine (Other) / Glycine
                      transport (Other) / Hippocampus (Other) /
                      N-methyl-D-aspartate receptors (Other)},
      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:41297659},
      doi          = {10.1016/j.pneurobio.2025.102856},
      url          = {https://pub.dzne.de/record/283021},
}