# Autophagy at the postsynapse begins with Rab11 and does not end with dendritic spine pruning

## TL;DR

This paper explores how autophagy starts at the postsynapse in neurons and challenges the idea that autophagosomes cause dendritic spine pruning.

## Contribution

The paper introduces Rab11 as a key player in autophagy initiation at dendritic spines and questions the role of autophagosomes in spine pruning.

## Key findings

- Rab11 maintains Atg9A in dendritic spines and is essential for LC3+ vesicle formation at the postsynapse.
- Autophagosomes may arise from NMDA receptor stimulation and local mTOR kinase activity.
- Autophagosomes are likely not responsible for dendritic spine pruning.

## Abstract

Neurons are highly differentiated and compartmentalized cells that conduct cellular processes in a spatiotemporally regulated manner. Autophagy in neurons occurs locally under stimulation and contributes to synaptic plasticity. Little is known about the initial steps leading to autophagy upon neuronal stimulation and the role of autophagic compartments at the postsynaptic part of the synapse. Here, we summarize our recent manuscript on Rab11 role in autophagy initiation in the dendritic spines. We showed that Rab11 maintains in the dendritic spines Atg9A and is necessary for LC3+ vesicles to emerge at the postsynapse. We hypothesize that autophagosomes arise due to an interplay between NMDA receptor stimulation and local mTOR kinase activity. We suggest that autophagosomes are not, in fact, responsible for dendritic spine pruning.