# Delineating how Calca neurons in the parabrachial nucleus mediate chronic pain

> **NIH NIH F30** · UNIVERSITY OF WASHINGTON · 2024 · $44,588

## Abstract

Project summary
Chronic pain is a highly prevalent and impactful condition. It persists past the time expected for normal tissue
healing from an acutely painful event, suggesting plasticity is occurring within the central nervous system to
perpetuate the pain experience. Furthermore, there are several conditions known to occur in the absence of
any tissue injury, such as fibromyalgia and tension-type headaches. Collectively, these conditions are referred
to as nociplastic pain syndromes. The broad goal of this proposal is to identify regions within the central
nervous system that exhibit plasticity in response to chronic pain. To model chronic pain, I will employ the
partial sciatic nerve ligation (pSNL). I will focus my investigation on the parabrachial nucleus (PBN), a hub for
the relay of aversive sensory information. My preliminary data suggests that the population of neurons
expressing Calca within the PBN exhibits an increase in neuronal activity acutely following chronic pain
induction, however this activity does not persist through the entire chronic pain experience. Additionally,
silencing the PBN Calca population prevents pSNL driven pain and chronically stimulating this population
produces pain that persists beyond stimulus cessation. Together this information informs my central hypothesis
that PBN Calca neurons are involved in the initiation and perpetuation of chronic pain. To test this hypothesis, I
will both manipulate Calca neurons and observe their activity during chronic pain. The experiments detailed in
Aim 1 will probe whether PBN Calca neurons are involved in maintaining the chronic pain experience by
assessing whether transient inhibition of PBN Calca neurons will ameliorate pSNL driven pain. Aim 2 will
explore how much and what type of stimulation is required for the manifestation of persistent pain driven by
PBN Calca neurons. This aim will also determine whether expression of the Calca gene is required for the
manifestation of chronic pain. Finally, in Aim 3 I will observe the activity of PBN Calca neurons preceding and
following the induction of chronic pain via calcium imaging. This will reveal when PBN Calca neurons exhibit
increased activity during a chronic pain experience. Collectively, these experiments will delineate the role
Calca neurons play in the manifestation and perpetuation of chronic pain. This work will further our
understanding of how chronic pain conditions arise and persist in the absence of a driving injury and may
suggest a target for novel pain therapies.

## Key facts

- **NIH application ID:** 10901885
- **Project number:** 5F30DA057845-02
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** Logan Francis Condon
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $44,588
- **Award type:** 5
- **Project period:** 2023-08-01 → 2027-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10901885

## Citation

> US National Institutes of Health, RePORTER application 10901885, Delineating how Calca neurons in the parabrachial nucleus mediate chronic pain (5F30DA057845-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10901885. Licensed CC0.

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