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@ARTICLE{Squadrani:270637,
      author       = {Squadrani, Lorenzo and Wert-Carvajal, Carlos and
                      Müller-Komorowska, Daniel and Bohmbach, Kirsten and
                      Henneberger, Christian and Verzelli, Pietro and
                      Tchumatchenko, Tatjana},
      title        = {{A}strocytes enhance plasticity response during reversal
                      learning.},
      journal      = {Communications biology},
      volume       = {7},
      number       = {1},
      issn         = {2399-3642},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2024-00809},
      pages        = {852},
      year         = {2024},
      abstract     = {Astrocytes play a key role in the regulation of synaptic
                      strength and are thought to orchestrate synaptic plasticity
                      and memory. Yet, how specifically astrocytes and their
                      neuroactive transmitters control learning and memory is
                      currently an open question. Recent experiments have
                      uncovered an astrocyte-mediated feedback loop in CA1
                      pyramidal neurons which is started by the release of
                      endocannabinoids by active neurons and closed by astrocytic
                      regulation of the D-serine levels at the dendrites. D-serine
                      is a co-agonist for the NMDA receptor regulating the
                      strength and direction of synaptic plasticity.
                      Activity-dependent D-serine release mediated by astrocytes
                      is therefore a candidate for mediating between long-term
                      synaptic depression (LTD) and potentiation (LTP) during
                      learning. Here, we show that the mathematical description of
                      this mechanism leads to a biophysical model of synaptic
                      plasticity consistent with the phenomenological model known
                      as the BCM model. The resulting mathematical framework can
                      explain the learning deficit observed in mice upon
                      disruption of the D-serine regulatory mechanism. It shows
                      that D-serine enhances plasticity during reversal learning,
                      ensuring fast responses to changes in the external
                      environment. The model provides new testable predictions
                      about the learning process, driving our understanding of the
                      functional role of neuron-glia interaction in learning.},
      keywords     = {Animals / Astrocytes: physiology / Astrocytes: metabolism /
                      Neuronal Plasticity: physiology / Mice / Reversal Learning:
                      physiology / Serine: metabolism / Models, Neurological /
                      Receptors, N-Methyl-D-Aspartate: metabolism / Serine (NLM
                      Chemicals) / Receptors, N-Methyl-D-Aspartate (NLM
                      Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {570},
      cid          = {I:(DE-2719)1013029},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38997325},
      pmc          = {pmc:PMC11245475},
      doi          = {10.1038/s42003-024-06540-8},
      url          = {https://pub.dzne.de/record/270637},
}