# Inhibitory Modulation and Circuitry in the Rostral Solitary Nucleus

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2021 · $331,500

## Abstract

PROJECT SUMMARY
The sense of taste profoundly affects food selection and is thus inextricably linked to health concerns including
caries exacerbated by sugar overconsumption and the sequela of obesity such as cardiovascular disease and
diabetes. Understanding how taste is represented and processed in the brain thus has important clinical
implications. The central processing of gustatory signals first occurs in the rostral nucleus of the solitary tract
(rNST). A major difficulty in discerning how taste is represented in this nucleus is phenotypic heterogeneity.
Output neurons are primarily glutamatergic and are responsible for representing the chemosensory properties
of tastants and relaying this information to circuits that affect perception, behavior, and reflexes, whereas
GABA/glycinergic neurons modulate the output cells. Due to technical challenges, it is thus far been impossible
to correlate taste response properties with neurotransmitter phenotype. Moreover, little is known about the
impact that GABAergic circuits exert on gustatory processing. Recent advances utilizing transgenic mice in
combination with optogenetics can overcome these barriers by introducing the light-sensitive protein
channelrhodopsin in specific cell types. This makes it possible to use neurophysiological recording techniques
to identify GABAergic neurons in vivo, based on responses to light, and to simultaneously describe
chemosensitive properties from the same cell. These techniques also allow temporally precise and repeatable
activation or deactivation of GABAergic circuitry. The present proposal will use strains of mice that express
either channelrhodopsin or archaerhodopsin in GABAergic neurons. Aim 1 will investigate the impact of
optogenetically induced GABAergic modulation on non-GABAergic neurons in vivo, and contrast GABAergic
modulation of rNST taste responses that arise from local neurons in the rNST, with those from the caudal NST,
a local medullary source of visceral signals, or from the central nucleus of the amygdala. Aim 2 will investigate
cellular mechanisms of GABAergic modulation in vitro combined with computational modeling to investigate
interactions between hyperpolarization-sensitive ion channels and inhibition. A second study will test the
hypothesis that inhibition differentially affects afferent signaling in neurons that contribute to an ascending
pathway compared to local reflexive pathways. Aim 3 will define properties of GABAergic neurons and
characterize subtypes. The first study will record in vivo from GAD65-ChR2 mice to identify GABAergic
neurons by responsiveness to light and test the hypothesis that the chemosensitive responses of GABAergic
rNST neurons differ from non-GABAergic neurons. A second aim will record in vitro from mice expressing
tdTomato in GAD65+ neurons to identify subtypes based on location, inhibitory modulation, and the presence
of the hyperpolarization-sensitive Ih current. A causal role for these currents in modula...

## Key facts

- **NIH application ID:** 10129336
- **Project number:** 5R01DC016112-05
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Susan P Travers
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $331,500
- **Award type:** 5
- **Project period:** 2017-04-01 → 2024-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10129336

## Citation

> US National Institutes of Health, RePORTER application 10129336, Inhibitory Modulation and Circuitry in the Rostral Solitary Nucleus (5R01DC016112-05). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10129336. Licensed CC0.

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