# Autophagy-dependent modulation of ER calcium release drives KCNMA1/BKCa signaling and seizure susceptibility

## TL;DR

This paper shows that autophagy helps control neuron activity by managing calcium release, and its loss increases seizure risk.

## Contribution

The study reveals a novel autophagy-dependent mechanism linking ER calcium release to BKCa channel activity in neurons.

## Key findings

- Autophagy restrains calcium-dependent signaling that connects ER calcium release to KCNMA1/BKCa activity.
- Loss of autophagy enhances this pathway, increasing seizure susceptibility in neurons.
- The study identifies a new regulatory role of autophagy in neuronal excitability.

## Abstract

Macroautophagy/autophagy is best known for its role in maintaining cellular homeostasis through degradation of damaged proteins and organelles. In neurons, autophagy also contributes to the regulation of activity by adjusting the availability of cellular components to physiological demand. In a recent study, we show that autophagy shapes neuronal excitability by restraining a calcium-dependent pathway that couples endoplasmic reticulum calcium release to KCNMA1/BKCa activity at the plasma membrane. When autophagy is lost, this pathway is enhanced, and seizure susceptibility increases.