# Modulation of attractive salt taste in Drosophila

## TL;DR

Flies reduce their attraction to salty food after eating salt, and this change is controlled by specific taste neurons.

## Contribution

The study identifies a cellular mechanism for modulating salt taste in flies, independent of gene transcription.

## Key findings

- A salt-enriched diet suppresses IR56b neuron activity to salt but not sucrose.
- Salt taste modulation is mediated by interoceptive mechanisms, not sensory adaptation.
- Modulation does not rely on IR56b transcriptional regulation or translational readthrough.

## Abstract

Modulating the palatability of salt is one way that animals regulate salt intake to promote fluid and ionic balance. In Drosophila melanogaster, low sodium attraction is primarily driven by “sweet” taste neurons that express the sodium-specific receptor IR56b. Here, we show that this appetitive sodium taste pathway is essential for tuning sodium attraction in response to prior salt consumption. Using in vivo calcium imaging, we find that a salt-enriched diet strongly suppresses the activity of IR56b neurons to salt but not to sucrose stimulation, demonstrating the existence of a sodium-specific modulatory mechanism in these cells. This effect is mediated by interoceptive mechanisms rather than sensory adaptation and does not depend on IR56b transcriptional regulation or differences in translational readthrough of a premature termination codon in the IR56b gene. This research provides a cellular basis for appetitive salt taste modulation and insight into mechanisms of salt homeostasis in the fly.

•A salt-enriched diet dramatically dampens appetitive salt taste in flies•Direct injection of a salt-containing buffer replicates this effect•Modulation appears specific to the salt receptor IR56b•Modulation does not depend on transcriptional regulation of IR56b

A salt-enriched diet dramatically dampens appetitive salt taste in flies

Direct injection of a salt-containing buffer replicates this effect

Modulation appears specific to the salt receptor IR56b

Modulation does not depend on transcriptional regulation of IR56b

Neurogenetics; neuroscience; sensory neuroscience