Dendritic autophagy degrades postsynaptic proteins and is required for long-term synaptic depression in mice.
Animals
Autophagy
/ genetics
Autophagy-Related Protein 5
/ genetics
Cells, Cultured
Dendritic Spines
/ physiology
Hippocampus
/ cytology
Long-Term Synaptic Depression
/ physiology
Male
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Neuronal Plasticity
/ physiology
Neurons
/ metabolism
Proteome
/ metabolism
Proteomics
/ methods
Pyramidal Cells
/ metabolism
Receptors, Metabotropic Glutamate
/ metabolism
Receptors, N-Methyl-D-Aspartate
/ metabolism
Synaptic Potentials
/ physiology
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
03 02 2022
03 02 2022
Historique:
received:
14
10
2020
accepted:
14
01
2022
entrez:
4
2
2022
pubmed:
5
2
2022
medline:
24
2
2022
Statut:
epublish
Résumé
The pruning of dendritic spines during development requires autophagy. This process is facilitated by long-term depression (LTD)-like mechanisms, which has led to speculation that LTD, a fundamental form of synaptic plasticity, also requires autophagy. Here, we show that the induction of LTD via activation of NMDA receptors or metabotropic glutamate receptors initiates autophagy in the postsynaptic dendrites in mice. Dendritic autophagic vesicles (AVs) act in parallel with the endocytic machinery to remove AMPA receptor subunits from the membrane for degradation. During NMDAR-LTD, key postsynaptic proteins are sequestered for autophagic degradation, as revealed by quantitative proteomic profiling of purified AVs. Pharmacological inhibition of AV biogenesis, or conditional ablation of atg5 in pyramidal neurons abolishes LTD and triggers sustained potentiation in the hippocampus. These deficits in synaptic plasticity are recapitulated by knockdown of atg5 specifically in postsynaptic pyramidal neurons in the CA1 area. Conducive to the role of synaptic plasticity in behavioral flexibility, mice with autophagy deficiency in excitatory neurons exhibit altered response in reversal learning. Therefore, local assembly of the autophagic machinery in dendrites ensures the degradation of postsynaptic components and facilitates LTD expression.
Identifiants
pubmed: 35115539
doi: 10.1038/s41467-022-28301-z
pii: 10.1038/s41467-022-28301-z
pmc: PMC8814153
doi:
Substances chimiques
Atg5 protein, mouse
0
Autophagy-Related Protein 5
0
Proteome
0
Receptors, Metabotropic Glutamate
0
Receptors, N-Methyl-D-Aspartate
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
680Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2022. The Author(s).
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