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

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.