# Mitochondrial Regulation of Nociceptor Function

> **NIH NIH R01** · UNIVERSITY OF NEW ENGLAND · 2024 · $389,347

## Abstract

Chronic pain affects more than 50 million Americans per year, resulting in extraordinary
personal and societal costs. Adding to the dilemma, deaths involving prescription opiate
analgesics have almost quadrupled in the last ten years. The clinical challenge of pain
management is underscored by evidence that chronic pain is mechanistically distinct from acute
pain, therefore a thorough understanding of the molecular and cellular mechanisms underlying
the transition to chronic pain is fundamental to improving and expanding treatment options.
Hyperalgesic priming is a compelling model of the transition to chronic pain in which an initial
injury resolves, but leaves the animal in a primed state in which a second insult induces a
greatly prolonged pain response. Experiments proposed here will examine the impact of
mitochondrial dynamics on the development of acute and chronic inflammatory pain compared
to a nerve injury model of neuropathic pain, and will explore molecular mechanisms mediating
proposed anti-nociceptive actions of endogenous uncoupling mechanisms and mitochondrial
uncoupling drugs. Specific Aim 1 will examine the how mitochondrial function changes in
response to noxious insult and the impact of mitochondrial regulation on acute hyperalgesia in
sensory ganglia. Specific Aim 2 will use patch clamp electrophysiology to demonstrate changes
in electrical properties of sensory neurons in response to manipulation of mitochondrial function,
and will identify cell signaling pathways that mediate mitochondrial effects on neuronal
excitability. Specific Aim 3 will characterize changes in mitochondrial function unique to the
transition to chronic pain, and will elucidate cell signaling pathways modulating the impact of
mitochondrial function on inflammatory and neuropathic pain chronification. This proposal will
use innovative approaches to explore novel mechanisms by which mitochondria influence the
manifestation of acute and chronic pain, and test the therapeutic potential of targeting these
mechanisms for pain relief.

## Key facts

- **NIH application ID:** 10783083
- **Project number:** 5R01NS131571-02
- **Recipient organization:** UNIVERSITY OF NEW ENGLAND
- **Principal Investigator:** DEREK C MOLLIVER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $389,347
- **Award type:** 5
- **Project period:** 2023-02-15 → 2028-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10783083

## Citation

> US National Institutes of Health, RePORTER application 10783083, Mitochondrial Regulation of Nociceptor Function (5R01NS131571-02). Retrieved via AI Analytics 2026-06-12 from https://api.ai-analytics.org/grant/nih/10783083. Licensed CC0.

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