NMDAR-dependent long-term depression is associated with increased short term plasticity through autophagy mediated loss of PSD-95.
Détails
Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_8A4FB9CDB826
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
NMDAR-dependent long-term depression is associated with increased short term plasticity through autophagy mediated loss of PSD-95.
Périodique
Nature communications
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
14/05/2021
Peer-reviewed
Oui
Volume
12
Numéro
1
Pages
2849
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Publication Status: epublish
Résumé
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.
Pubmed
Open Access
Oui
Création de la notice
25/05/2021 14:54
Dernière modification de la notice
12/01/2022 8:11