% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Henneberger:164287,
      author       = {Henneberger, Christian and Bard, Lucie and Panatier, Aude
                      and Reynolds, James P and Kopach, Olga and Medvedev, Nikolay
                      I and Minge, Daniel and Herde, Michel K and Anders, Stefanie
                      and Kraev, Igor and Heller, Janosch P and Rama, Sylvain and
                      Zheng, Kaiyu and Jensen, Thomas P and Sanchez-Romero,
                      Inmaculada and Jackson, Colin J and Janovjak, Harald and
                      Ottersen, Ole Petter and Nagelhus, Erlend Arnulf and Oliet,
                      Stephane H R and Stewart, Michael G and Nägerl, U Valentin
                      and Rusakov, Dmitri A},
      title        = {{LTP} {I}nduction {B}oosts {G}lutamate {S}pillover by
                      {D}riving {W}ithdrawal of {P}erisynaptic {A}stroglia.},
      journal      = {Neuron},
      volume       = {108},
      number       = {5},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2022-00941},
      pages        = {919 - 936.e11},
      year         = {2020},
      abstract     = {Extrasynaptic actions of glutamate are limited by
                      high-affinity transporters expressed by perisynaptic
                      astroglial processes (PAPs): this helps maintain
                      point-to-point transmission in excitatory circuits. Memory
                      formation in the brain is associated with synaptic
                      remodeling, but how this affects PAPs and therefore
                      extrasynaptic glutamate actions is poorly understood. Here,
                      we used advanced imaging methods, in situ and in vivo, to
                      find that a classical synaptic memory mechanism, long-term
                      potentiation (LTP), triggers withdrawal of PAPs from
                      potentiated synapses. Optical glutamate sensors combined
                      with patch-clamp and 3D molecular localization reveal that
                      LTP induction thus prompts spatial retreat of astroglial
                      glutamate transporters, boosting glutamate spillover and
                      NMDA-receptor-mediated inter-synaptic cross-talk. The
                      LTP-triggered PAP withdrawal involves NKCC1 transporters and
                      the actin-controlling protein cofilin but does not depend on
                      major Ca2+-dependent cascades in astrocytes. We have
                      therefore uncovered a mechanism by which a memory trace at
                      one synapse could alter signal handling by multiple
                      neighboring connections.},
      keywords     = {Animals / Astrocytes: metabolism / Astrocytes:
                      ultrastructure / Female / Glutamic Acid: metabolism /
                      Imaging, Three-Dimensional: methods / Long-Term
                      Potentiation: physiology / Male / Mice / Mice, Inbred C57BL
                      / Mice, Knockout / Mice, Transgenic / Organ Culture
                      Techniques / Rats / Rats, Sprague-Dawley / Rats, Wistar /
                      Synapses: metabolism / Synapses: ultrastructure / Excitatory
                      synapse (Other) / astrocyte plasticity (Other) / barrel
                      cortex (Other) / glutamate sensor imaging (Other) /
                      glutamate spillover (Other) / hippocampus (Other) /
                      long-term potentiation (Other) / perisynaptic astroglial
                      processes (Other) / super-resolution microscopy (Other) /
                      whisker stimulation (Other) / Glutamic Acid (NLM Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {610},
      cid          = {I:(DE-2719)1013029},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32976770},
      pmc          = {pmc:PMC7736499},
      doi          = {10.1016/j.neuron.2020.08.030},
      url          = {https://pub.dzne.de/record/164287},
}