How nerve and blood vessel interactions cause neuropathic spontaneous pain
Neuron vasculature interactions in pain
This work looks at how nerve cells and nearby blood vessels interact to cause spontaneous nerve pain after injury, with the goal of helping people who have neuropathic pain.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Cincinnati NIH-funded |
| Lab location | 1 site (Cincinnati, United States) |
| Project ID | NIH-11187154 on NIH RePORTER |
What this research studies
Researchers will use genetically modified mice whose sensory nerve cells light up when active so they can watch nerve activity inside the dorsal root ganglia after nerve injury. They have found clusters of nerve cells that fire on their own after injury and that these cluster firings link to spontaneous pain behaviors in mice. The team will test how activation of the sympathetic nervous system and adrenergic signaling (the body's fight-or-flight chemicals) change these cluster patterns and whether blocking those signals stops the abnormal firing. They will work to determine whether the key targets are the sensory neurons themselves or nearby blood vessels in the ganglia, which could point to different treatment strategies.
Who could benefit from this research
Good fit: People with neuropathic pain from nerve injury who experience ongoing spontaneous pain (not only pain from touch or movement) would be the most relevant group for future trials or related clinical efforts.
Not a fit: People whose pain is purely musculoskeletal, inflammatory, or centrally driven (not due to peripheral nerve injury) are less likely to benefit from the findings.
Why it matters
Potential benefit: If successful, this work could point to new treatment targets — for example drugs that block adrenergic signaling or modify nerve–blood vessel interactions — to reduce hard-to-treat spontaneous neuropathic pain.
How similar studies have performed: Prior mouse work by collaborating labs has shown clustered DRG neuron activity links to spontaneous pain and can be reduced by adrenergic blockers, but human evidence and clinical translation remain limited.
Where this research is happening
Cincinnati, United States
- University of Cincinnati — Cincinnati, United States (Active)
Researchers
- Principal investigator: Zhang, Jun-Ming — University of Cincinnati
- Study coordinator: Zhang, Jun-Ming
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.