Bin Pan
University of Texas Medical Branch at Galveston, TX·Neuroscience
Chronic pain that persists after an injury has healed is common and poorly treated. Opioids relieve pain in the short term but often lead to addiction and side effects that patients cannot tolerate, so there is a strong push to find pain targets that work by a different route.
- Fields
Neuroscience
Pharmacology
Physiology
- Topics
chronic pain
neuropathic pain
osteoarthritis pain
- Grants
- 1 known grant, through Apr 2028
What they work on
- Establish whether CaMKII activity in peripheral sensory neurons suppresses pain, testing the hypothesis that reduced CaMKII signaling in dorsal root ganglion neurons maintains chronic pain in preclinical neuropathic and osteoarthritic pain models.
- Identify the anatomic site where sensory neuron CaMKII produces its pain-relieving effect, using viral approaches designed to target CaMKII selectively in primary sensory neurons of the dorsal root ganglion.
- Determine the molecular mechanisms by which painful conditions inactivate CaMKII, the calcium/calmodulin-dependent kinase that tunes excitable cell activity, in animal and cell models of pain.
- Test whether amplifying sensory neuron CaMKII signaling by molecular tools or by dorsal root ganglion electrical neuromodulation produces analgesia, as proof of concept for opioid-free pain treatment.
More about the research
One clue comes from a therapy already used in patients: electrically stimulating the dorsal root ganglia, the clusters of sensory nerve cell bodies just outside the spinal cord that relay touch and pain signals from the body, can block pain in both patients and animal models. Because that treatment works, the molecules it acts through are promising drug targets. This project pursues one of them, a protein kinase that reads calcium signals inside nerve cells.
Why it matters
Chronic neuropathic and arthritis pain affect large numbers of people, and the main available drugs, opioids, carry risks of addiction and severe side effects. If reduced CaMKII activity in peripheral sensory neurons turns out to sustain chronic pain, selectively restoring that activity, whether by molecular means or by electrical stimulation of the dorsal root ganglion, could become a non-opioid route to pain relief.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Hayley McLoughlin
University of Michigan, MI·Neuroscience
Characterize the onset and progression of peripheral neuropathy in two SCA3 mouse models using functional nerve assessments alongside histological analysis of peripheral nerve tissue.
Kevin Tidgewell
University of Kentucky, KY·Pharmacology
Isolate bioactive compounds from Cameroonian medicinal plants such as Paullinia pinnata by fractionating extracts and testing each fraction for binding to sigma-2/TMEM97, a calcium-regulating protein linked to pain.
Huijuan Hu
Rutgers University-New Brunswick, NJ·Neuroscience
Determine whether deleting or knocking down STIM2, a calcium-store sensor, in the mouse spinal cord reduces chronic itch in models of chronic itch, including DNFB- and DCP-induced dermatitis.
The school
University of Texas Medical Branch at Galveston: 14 labs on PI Pages, $241M a year on research, 141 research doctorates a year.
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