# Project 4 - Queme

> **NIH NIH P20** · UNIVERSITY OF NEW ENGLAND · 2024 · $253,362

## Abstract

SUMMARY
For a long time, it has been known that there is a strong link between chronic pain and high levels of stress and anxiety.
High levels of stress are a risk factor for developing chronic post-surgical pain. It remains unclear if and how stress can
facilitate the transition from acute to chronic pain. In the periphery, pain is perceived by primary sensory neurons, whose
cell bodies reside in the dorsal root ganglia, where each sensory neuron is enveloped by satellite glial cells, a non-neuronal
support cell. Previous studies show that peripheral injury as well as stress may induce satellite glial cell (SGC) activation,
a phenomenon characterized by increased expression of glial fibrillary acidic protein, changes in gene expression, and
release of pro-nociceptive signaling molecules. SGC activation has been linked to the development of mechanical
hyperalgesia and primary afferent sensitization in a variety of rodent models. Our objective is to characterize the how
stress and/or peripheral injury-induced satellite glial cell activation may modulate primary afferent sensitization and lead
to the development of prolonged ischemic muscle pain. To explore this, the proposed research will use novel mouse
model of stress based on loss of environmental enrichment (LEE). This model does not employ the potential confounder
of noxious physical stimulation. Our preliminary data shows that LEE induced stress results in mechanical hyperalgesia
before injury and increased pain-related behaviors after an ischemia with reperfusion injury (I/R). We hypothesize that
LEE+(I/R)-induced satellite glial cell activation induces peripheral sensitization via increased expression and
release of pro-nociceptive signaling molecules that may modulate the development of chronic pain after injury. We
will use RNA sequencing, bioinformatics, animal behavior and ex-vivo electrophysiology to characterize how SGC
modulate pain perception after I/R in the context of stress. Aim 1 Characterize the transcriptomic changes in I/R induced
SGC activation and the signaling molecules that mediate muscle afferent sensitivity in the presence or absence of stress.
Transcriptomic changes in activated satellite glial cells after injury, stress, or a combination of both have never been
thoroughly characterized. The proposed RNAseq experiments and bioinformatics analysis on these data will allow us to better
characterize how gene expression changes in SGCs mediates pain development. Aim 2 will explore how SGC activation impacts
the function of muscle primary sensory neurons. We will use a combination of behavior, ex-vivo electrophysiology, and
calcium imaging to determine the changes in muscle primary afferent function that are mediated by SGC activation after stress
and/or injury. The data from these studies will become the cornerstone of a research program focused on how stress facilitates
the transition from acute to chronic pain and the specific role that SGCs play in this process and wil...

## Key facts

- **NIH application ID:** 10771610
- **Project number:** 1P20GM152330-01
- **Recipient organization:** UNIVERSITY OF NEW ENGLAND
- **Principal Investigator:** Luis Fernando Queme Cobar
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $253,362
- **Award type:** 1
- **Project period:** 2024-01-01 → 2028-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10771610

## Citation

> US National Institutes of Health, RePORTER application 10771610, Project 4 - Queme (1P20GM152330-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10771610. Licensed CC0.

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