University of Cincinnati College of Medicine

A “bench to bedside” translational pain research program has been established in the Department of Anesthesiology at the University of Cincinnati to foster the development of medical students, residents, fellows, and clinical faculty who are interested in an academic career. We have assembled a team that combines well-funded basic science researchers, clinical anesthesiologists, and nurse coordinators with complementary expertise and training backgrounds.

Ongoing projects in our department include NIH-funded preclinical research on mechanisms of pain and itch, and clinical studies including chart review studies and clinical trials to translate lab findings into improved clinical pain management.

Steroids and steroid receptors in pain management (Jun-Ming Zhang Lab)

This project is funded by NIAMS and the University of Cincinnati to further understanding of how steroid receptors in the sensory nervous system change in pathological conditions, and how such changes may alter responses to steroid treatments for chronic pain conditions. Ultimately, we expect to develop new treatment regimens to maximize the beneficial effects and to decrease the side effects associated with steroid treatment in human patients.

Pathological pain: mechanisms and management (Jun-Ming Zhang Lab)

Several projects funded by NINDS, Air Force/DoD, and the University of Cincinnati to explore the mechanisms of pathological pain such as chronic low back pain and CRPS. Specifically, we are interested understanding how immune responses and inflammation are regulated by the sympathetic nervous system, how obesity and diet may alter postoperative pain, and how nerve regeneration is related to persistent neuropathic pain. Ongoing clinical trials aim to determine whether extended block of the injured nerve will lower the risk of developing chronic pain, and to identify biomarkers that can be used to predicate the outcomes of sympathetic block for CRPS patients.

Preclinical study of pediatric pain (Mark Baccei Lab)

Several projects funded by NINDS to investigate neurological mechanisms of pediatric pain. One of the projects carried out by Dr. Baccei’s group is aimed to identify the role of voltage-independent (“i.e. “leak”) ion channels in shaping the excitability of spinal projection neurons, which are responsible for conveying nociceptive signals to the brain and are known to be essential for pain sensation. The project will also elucidate how activity in these key output neurons during early life regulates the maturation of sensory inputs originating from skin and muscle, with the goal of advancing our understanding of the mechanistic basis for musculoskeletal pain in the pediatric population. Another project focuses on exploring the neurobiological mechanisms by which neonatal tissue damage can “prime” developing pain pathways, such that an exacerbated degree of pain hypersensitivity is observed following repeat injury later in life. Specifically, this project will test the hypothesis that neonatal injury causes persistent deficits in synaptic inhibition onto adult spinal projection neurons, which result in an amplification of ascending pain signaling to the brain.

Neuroinflammation and chronic pain (Temugin Berta Lab)

This project is funded by the University of Cincinnati to explore the neuroinflammatory mechanisms underlying chronic pain. Current pain drugs are disappointing and mostly target neuronal pathways and general symptoms of chronic pain. However, it is now clear that chronic pain is a neuroinflammatory disease associated with mechanisms that overlap both the nervous and the immune systems. Dr. Berta’s group has investigated how microglial cells in the central nervous system regulate chronic pain. They are now focusing on how individual neuronal, glial and immune cells process information and interact in the peripheral nervous system to mount and resolve neuroinflammatory responses. Eventually, this research may lead to innovative therapeutic approaches and improved clinical treatments of chronic pain.

Central and peripheral mechanisms of pain and itch (Steve Davidson Lab)

Funded by the American Pain Society and the Rita Allen Foundation, NIAMS, and University of Cincinnati, the group led by Dr. Davidson explores central and peripheral mechanisms of pain in animal models and human sensory neurons. One of the projects is to characterize limbic circuits in pain and itch by examining the supraspinal mechanisms of pain processing with the specific goal of identifying and manipulating the neurons and circuits involved in modulating pain tolerance. The hypothesis is that chronic pain and itch may be controlled through non-opioid interventions by modulating the activity in brain regions that regulate emotional responses to pain and itch. In this way, tolerance to pain and itch may be enhanced and quality of life improved. Another project is aimed to examining physiology of human sensory neurons. This project advances an innovative method for the recovery and cell-culture of primary human sensory neurons. Rodent models are the standard research tool in basic science; however, difficulty in translation has stymied the success of new analgesics. Therefore, the main goal of this project is to determine the function and gene expression profile of individual human sensory neurons that are responsible for carrying information about pain and itch from the periphery to the central nervous system. It is hypothesized that by using human primary neurons we will enhance the translational potential of novel therapeutic agents that eventually move to clinical trials.