Basic Research

The Department of Anesthesiology performs cutting-edge research on the neurobiology of pain and somatosensation through the Pain Research Center. Center laboratories and core research facilities are housed together in the CARE/Crawley Building. Laboratories are equipped to investigate critical questions in anesthesia and pain research such as the mechanisms of nerve regeneration and nociceptive pathway development, opioid and non-opioid analgesia, neural-immune interactions, and brain circuitry to control pain. 

Principal Investigators:

Jun-Ming Zhang, MSc, MD

Study of Activity-Dependent Sympathetic Sprouting

Neuropathic pain conditions such as CRPS are common and intractable. We propose to continue the study of sympathetic component in neuropathic pain. Using a rat/mouse model, we will determine how abnormal activity, inflammation, ATP release affect sympathetic outgrowth and the neurons that sense pain.

Neural and Chemical Basis of Pathologic Pain

Chronic pain conditions are common, long-lasting, and debilitating. In this project, we propose to study the newly recognized role of inflammation and Nav1.6 sodium channel isoform in chronic pain. Using a rat model, we will determine how Nav1.6 and GRO/KC (known as interlukin-8 in human) directly affects the neurons that sense pain.

Mark Baccei, PhD

Although infants and children experience considerable pain as the result of injury, disease, surgery or intensive care therapy, pediatric pain remains under-treated and poorly understood. Efforts to design new, evidence-based treatments for chronic pediatric pain have been hampered by a lack of information regarding how neonatal pain circuits in the CNS respond to tissue damage at a cellular and molecular level.

My lab is currently characterizing the short- and long-term consequences of tissue injury during early life for the function of developing synaptic networks in the superficial dorsal horn of the spinal cord, which serves as an important relay station in the pain pathway.

Experimental approaches include in vitro electrophysiology in rodent spinal cord slices, immunohistochemistry, Western blotting, and behavioral measurements of pain sensitivity. It is our hope that by identifying age-specific changes in synaptic organization within central pain networks under pathological conditions, this work will yield new insight into the underlying basis for hyperalgesia during the early postnatal period and also help explain why neonatal tissue damage appears exclusively capable of altering pain perception throughout life.

Steve Davidson, PhD

Physiological studies of opioid and non-opioid analgesics in human peripheral nervous system.

Most analgesics are generated through research and development efforts in animal models, but never tested in humans prior to clinical trials. Our lab has pioneered a technique permitting investigation of human nerve function in vitro to assess excitability and pain relieving properties of drugs prior to expensive and risky clinical trials. 

Modulation of pain and itch via control of thalamo-cortical circuitry. 

The experience of pain and itch requires neural processing within the brain, yet much is still unknown about the precise neural circuitry leading to the unpleasant sensory and emotional qualities generated by this experience. Our lab uses electrophysiological, optogenetic, and behavioral strategies to probe the circuits connecting the thalamus to the limbic cortex which we hypothesize regulate the affective, motivational, and cognitive qualities of pain and itch. Our goal is to establish the ability to modulate neural activity within these circuits which we anticipate will lead to new strategies to enhance patients' control over pain and capacity to cope.

Temugin Berta, PhD

Neuroinflammation and chronic pain.

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. We have investigated how microglial cells in the central nervous system regulate chronic pain. We 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.