# Determining the Function of TRPC3 in Allergic Contact Dermatitis Induced Itch

> **NIH NIH F31** · UNIVERSITY OF PENNSYLVANIA · 2020 · $32,732

## Abstract

Project Summary
The definition of itch as an irritating sensation that triggers the desire to scratch does not fully capture the
impact on people suffering from acute and chronic itch (personal discomfort, inattention, insomnia, medical
expenses, and lost work). Previous studies have highlighted the important role of TRP channels, such as
TRPV1 and TRPA1, in a variety of sensory pathways including itch. In this proposal, I aim to provide a better
understanding of the pathophysiology underlying itch by examining the role of the TRP channel, TRPC3, in a
mouse model of allergic contact dermatitis. Previously published data from our lab found TrpC3 null mice
exhibited no phenotypic differences in a variety of behavioral tests for acute pain and itch sensation. My
preliminary behavioral studies have shown that TrpC3 knock out mice display greater scratching behavior in
response to the mouse model of allergic contact dermatitis (ACD), termed contact hypersensitivity (CHS),
when compared to wild type controls. Since TrpC3 is known to be expressed in dorsal root ganglion neurons,
cholinergic neurons, glutamatergic neurons, and T cells, I hypothesize that TrpC3 antagonizes itch sensation
through one of these cell types. In Aim 1, I will confirm the expression pattern of TrpC3 in the nervous system
and immune system and determine whether changes in expression occur with CHS by utilizing real time PCR
and in situ hybridization. Additionally, I will characterize the infiltration of immune cells in the affected skin of
mice with CHS (TRPC3 KO and WT mice) through skin histology and flow cytometry. In Aim 2, I will determine
whether TRPC3 modulates itch in ACD through its expression in neuronal and immune cells, using TrpC3
conditional KO mice. Specifically, I will create neuronal and immune cell TrpC3 conditional knock out mouse
lines to determine which cell types require TrpC3 expression to suppress itch sensation in ACD under normal
conditions by examining the scratching behavior. To target TrpC3 expression in neuronal cells, I will generate
three TrpC3 conditional KO lines using Synapsin1Cre (all neurons), ChATiCre (cholinergic neurons), and
VGLUT2Cre (glutamatergic neurons) genetic alleles. To target TrpC3 expression in immune cells, I will use the
hematopoietic Cre line, Vav1-iCre drivers. Successful completion of the proposed aims will provide critical
insight into the role of TRPC3 in antagonizing itch sensation in ACD and will propel further cellular and
molecular studies to identify the pathophysiology of itch. The results of this project have the potential to impact
treatment outcomes and is applicable to a significant portion of the population who suffer from ACD and
chronic itch.

## Key facts

- **NIH application ID:** 9939277
- **Project number:** 5F31AR075436-02
- **Recipient organization:** UNIVERSITY OF PENNSYLVANIA
- **Principal Investigator:** Katherine Beattie
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $32,732
- **Award type:** 5
- **Project period:** 2019-04-01 → 2021-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9939277

## Citation

> US National Institutes of Health, RePORTER application 9939277, Determining the Function of TRPC3 in Allergic Contact Dermatitis Induced Itch (5F31AR075436-02). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9939277. Licensed CC0.

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