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NMDAR-dependent long-term depression is associated with increased short term plasticity through autophagy mediated loss of PSD-95

Author

Listed:
  • Benjamin Compans

    (Univ. Bordeaux, IINS, UMR 5297)

  • Come Camus

    (Univ. Bordeaux, IINS, UMR 5297)

  • Emmanouela Kallergi

    (University of Lausanne)

  • Silvia Sposini

    (Univ. Bordeaux, IINS, UMR 5297)

  • Magalie Martineau

    (Univ. Bordeaux, IINS, UMR 5297)

  • Corey Butler

    (Univ. Bordeaux, IINS, UMR 5297)

  • Adel Kechkar

    (Univ. Bordeaux, IINS, UMR 5297)

  • Remco V. Klaassen

    (Department Molecular and Cellular Neurobiology)

  • Natacha Retailleau

    (Univ. Bordeaux, IINS, UMR 5297)

  • Terrence J. Sejnowski

    (Howard Hughes Medical Institute, Salk Institute for Biological Studies)

  • August B. Smit

    (Department Molecular and Cellular Neurobiology)

  • Jean-Baptiste Sibarita

    (Univ. Bordeaux, IINS, UMR 5297)

  • Thomas M. Bartol

    (Howard Hughes Medical Institute, Salk Institute for Biological Studies)

  • David Perrais

    (Univ. Bordeaux, IINS, UMR 5297)

  • Vassiliki Nikoletopoulou

    (University of Lausanne)

  • Daniel Choquet

    (Univ. Bordeaux, IINS, UMR 5297
    Univ. Bordeaux, CNRS, INSERM, Bordeaux Imaging Center, BIC, UMS 3420)

  • Eric Hosy

    (Univ. Bordeaux, IINS, UMR 5297)

Abstract

Long-term depression (LTD) of synaptic strength can take multiple forms and contribute to circuit remodeling, memory encoding or erasure. The generic term LTD encompasses various induction pathways, including activation of NMDA, mGlu or P2X receptors. However, the associated specific molecular mechanisms and effects on synaptic physiology are still unclear. We here compare how NMDAR- or P2XR-dependent LTD affect synaptic nanoscale organization and function in rodents. While both LTDs are associated with a loss and reorganization of synaptic AMPARs, only NMDAR-dependent LTD induction triggers a profound reorganization of PSD-95. This modification, which requires the autophagy machinery to remove the T19-phosphorylated form of PSD-95 from synapses, leads to an increase in AMPAR surface mobility. We demonstrate that these post-synaptic changes that occur specifically during NMDAR-dependent LTD result in an increased short-term plasticity improving neuronal responsiveness of depressed synapses. Our results establish that P2XR- and NMDAR-mediated LTD are associated to functionally distinct forms of LTD.

Suggested Citation

  • Benjamin Compans & Come Camus & Emmanouela Kallergi & Silvia Sposini & Magalie Martineau & Corey Butler & Adel Kechkar & Remco V. Klaassen & Natacha Retailleau & Terrence J. Sejnowski & August B. Smit, 2021. "NMDAR-dependent long-term depression is associated with increased short term plasticity through autophagy mediated loss of PSD-95," Nature Communications, Nature, vol. 12(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-23133-9
    DOI: 10.1038/s41467-021-23133-9
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    Cited by:

    1. Emmanouela Kallergi & Akrivi-Dimitra Daskalaki & Angeliki Kolaxi & Come Camus & Evangelia Ioannou & Valentina Mercaldo & Per Haberkant & Frank Stein & Kyriaki Sidiropoulou & Yannis Dalezios & Mikhail , 2022. "Dendritic autophagy degrades postsynaptic proteins and is required for long-term synaptic depression in mice," Nature Communications, Nature, vol. 13(1), pages 1-23, December.

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