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

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, Jean-Baptiste Sibarita, Thomas M. Bartol, David Perrais, Vassiliki Nikoletopoulou, Daniel Choquet and Eric Hosy ()
Additional contact information
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
Eric Hosy: Univ. Bordeaux, IINS, UMR 5297

Nature Communications, 2021, vol. 12, issue 1, 1-18

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-23133-9

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