In brief:Kallergi, Daskalaki and colleagues demonstrate that autophagy is cell autonomously required in pyramidal excitatory neurons for the induction of long-term synaptic depression (LTD). They uncover the novel and local biogenesis of autophagic vesicles (AVs) in dendrites upon LTD, by which post-synaptic components are rapidly accessible on-site for autophagic degradation. Using quantitative proteomics on purified AVs, they reveal that upon LTD the autophagic cargo is enriched in synaptic, cytoskeletal and autism-implicated proteins.
Highlights Autophagy is required cell-autonomously in pyramidal neurons for LTD. NMDAR-and mGluR-mediated LTD trigger the local biogenesis of autophagic vesicles in dendrites. Autophagic vesicles sequester primarily synaptic and cytoskeletal cargo upon LTD. Mild impairment in autophagy leads to deficits in cognitive flexibility.
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