# Central mechanisms of itch transmission

> **NIH NIH R01** · WASHINGTON UNIVERSITY · 2021 · $490,219

## Abstract

Abstract
Chronic itch is an unmet medical problem associated with numerous skin, immune, and nervous diseases. An
imbalance of excitatory and inhibitory transmission of itch may contribute to the etiology of chronic itch.
Understanding of inhibitory mechanisms of itch transmission is important for developing targeted anti-itch
therapies. The spinal cord interneurons expressing gastrin-releasing peptide receptor (GRPR) are crucial for itch
transmission. Recent studies suggest that a subset of inhibitory neurons expressing neurokinin 3 receptor
(TacR3) may be activated by pain for itch inhibition. We will employ an interdisciplinary approach to test the
hypothesis that TacR3 inhibitory neurons inhibit itch but not pain by inhibiting GRPR neurons. Aim 1 will
determine anatomic and electrophysiological properties of TacR3 inhibitory neurons. Aim 2 will determine the
role of spinal TacR3 inhibitory neurons in itch inhibition. Aim 3 will determine whether TacR3 neurons inhibit
GRPR neurons via GABAergic transmission. These studies should yield fundamental insight onto the spinal
mechanisms by which itch is inhibited by pain.

## Key facts

- **NIH application ID:** 10116893
- **Project number:** 1R01NS113938-01A1
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** ZHOUFENG CHEN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $490,219
- **Award type:** 1
- **Project period:** 2021-02-01 → 2025-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10116893

## Citation

> US National Institutes of Health, RePORTER application 10116893, Central mechanisms of itch transmission (1R01NS113938-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10116893. Licensed CC0.

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