# Activation of 5-HT1A autoreceptors causes actin depolymerization in Drosophila serotonergic neurons

## TL;DR

This study explores how serotonin receptors affect axon growth in fruit fly neurons, finding that they cause actin structures to break down.

## Contribution

The study reveals a novel cellular mechanism linking 5-HT1A autoreceptor activation to actin depolymerization in serotonergic neurons.

## Key findings

- Activation of 5-HT1A increases G/F-actin ratios in Drosophila serotonergic neurons.
- 5-HT1A negatively regulates axon outgrowth through actin depolymerization.

## Abstract

Serotonergic neurons extend long, highly branched axons throughout the brain during development and are responsible for the modulation of many behaviors. Because proper behavioral output is dependent on precise outgrowth and targeting of serotonergic axons, it is important to understand how serotonergic axon outgrowth is regulated during development. Our previous pharmacological experiments suggest that autoreceptor 5-HT1A negatively regulates axon outgrowth and branching of
Drosophila
serotonergic neurons
in vitro
, though the cellular mechanisms are unknown. Here we show that pharmacological activation of 5-HT1A leads to increases in G/F-actin ratios, suggesting 5-HT1A negatively regulates serotonergic axon outgrowth through actin depolymerization.