Format

Send to

Choose Destination
Neuron. 2014 Nov 19;84(4):806-20. doi: 10.1016/j.neuron.2014.09.032. Epub 2014 Oct 30.

Independent, reciprocal neuromodulatory control of sweet and bitter taste sensitivity during starvation in Drosophila.

Author information

1
Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA; Janelia Farm Research Campus, HHMI, Ashburn, VA 20147, USA. Electronic address: inagakih@janelia.hhmi.org.
2
Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA.
3
Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA; Howard Hughes Medical Institute. Electronic address: wuwei@caltech.edu.

Abstract

An organism's behavioral decisions often depend upon the relative strength of appetitive and aversive sensory stimuli, the relative sensitivity to which can be modified by internal states like hunger. However, whether sensitivity to such opposing influences is modulated in a unidirectional or bidirectional manner is not clear. Starved flies exhibit increased sugar and decreased bitter sensitivity. It is widely believed that only sugar sensitivity changes, and that this masks bitter sensitivity. Here we use gene- and circuit-level manipulations to show that sweet and bitter sensitivity are independently and reciprocally regulated by starvation in Drosophila. We identify orthogonal neuromodulatory cascades that oppositely control peripheral taste sensitivity for each modality. Moreover, these pathways are recruited at increasing hunger levels, such that low-risk changes (higher sugar sensitivity) precede high-risk changes (lower sensitivity to potentially toxic resources). In this way, state-intensity-dependent, reciprocal regulation of appetitive and aversive peripheral gustatory sensitivity permits flexible, adaptive feeding decisions.

PMID:
25451195
PMCID:
PMC4365050
DOI:
10.1016/j.neuron.2014.09.032
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center