Nature Communications (Oct 2017)

Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice

  • Elisabetta Aloisi,
  • Katy Le Corf,
  • Julien Dupuis,
  • Pei Zhang,
  • Melanie Ginger,
  • Virginie Labrousse,
  • Michela Spatuzza,
  • Matthias Georg Haberl,
  • Lara Costa,
  • Ryuichi Shigemoto,
  • Anke Tappe-Theodor,
  • Filippo Drago,
  • Pier Vincenzo Piazza,
  • Christophe Mulle,
  • Laurent Groc,
  • Lucia Ciranna,
  • Maria Vincenza Catania,
  • Andreas Frick

DOI
https://doi.org/10.1038/s41467-017-01191-2
Journal volume & issue
Vol. 8, no. 1
pp. 1 – 14

Abstract

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Dysfunction of mGluR5 has been implicated in Fragile X syndrome. Here, using a single-molecule tracking technique, the authors found an increased lateral mobility of mGluR5 at the synaptic site in Fmr1 KO hippocampal neurons, leading to abnormal NMDAR-mediated synaptic plasticity and cognitive deficits.