# Characterization of Taste-independent Sugar Sensor in the Brain

> **NIH NIH R01** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2020 · $419,840

## Abstract

Project Description
Feeding behavior is influenced by multiple factors including food palatability and
nutritional needs. Peripheral chemosensory taste neurons primarily detect palatable
food, but animals lacking these taste neurons can still develop a preference to sugars on
the basis of their nutritional value. My laboratory previously determined that dSLC5A11+,
EB R4d neurons in the Drosophila brain are required for the selection of nutritive D-
glucose over nonnutritive L-glucose after periods of starvation. dSLC5A11 (or cupcake)
acts on approximately 12 pairs of EB R4d neurons to trigger the selection of nutritive
sugars, but the mechanism underlying this process is not understood. We previously
proposed two possible mechanisms by which EB R4 neurons may mediate the selection
of nutritive sugars: (1) by detecting the nutritional value of sugar through direct activation
or (2) monitoring the internal energy reserves of the fly with a direct nutrient sensor
located elsewhere; starved flies lacking functional EB R4d neurons cannot sense the
deprived metabolic state and, thus, would not select nutritive sugars.
 Through calcium imaging and a more-sensitive electrophysiology approach, we
tested whether EB R4d neurons respond to nutritive sugars, but failed to observe any
responses to glucose or any other sugars. Instead, the activity of EB R4d neurons and
the expression of dSLC5A11 transcript increase significantly following periods of
starvation. Furthermore, the increased dSLC5A11 suppresses dKCNQ currents, thereby
increasing the activity of EB R4d neurons during starvation. Recently, we found that EB
R4d neurons are robustly activated by serotonin, which is apparently secreted by the
neurons labeled by R50H05-GAL4. These R50H05+ neurons were shown to promote
food intake, similar to EB R4d neurons. We also found that another population of the EB
Ring neurons, apparently the neighboring EB R4m neurons, suppress food intake.
 In this renewal application, we propose to study the following questions based on
our published and preliminary results. In Aim 1, we will determine the mechanisms by
which EB R4d neurons are activated. We will further elucidate the dSLC5A11/dKCNQ-
mediated mechanism, but also investigate the dSLC5A11–independent mechanism in
which serotonin plays critical roles in stimulating the activity of EB R4d neurons and the
expression of dSLC5A11 transcript. In Aim 2, we will determine whether EB R4d
neurons function downstream of R50H05+ neurons. In Aim 3, we will validate that the
recently identified EB R4m neurons suppress food intake and characterize the
interactions between EB R4m and EB R4d neurons, and between EB R4d or EB R4m
neurons, and the sleep-promoting EB R2 neurons.

## Key facts

- **NIH application ID:** 9853778
- **Project number:** 5R01DK116294-08
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** HYUNG D RYOO
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $419,840
- **Award type:** 5
- **Project period:** 2012-09-13 → 2022-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9853778

## Citation

> US National Institutes of Health, RePORTER application 9853778, Characterization of Taste-independent Sugar Sensor in the Brain (5R01DK116294-08). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9853778. Licensed CC0.

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