Today is Saturday, Jan. 20, 2018

Department of


Basic Research

Below is some of our most active basic science research.

Jun-Ming Zhang, MSc, MD

Study of Activity-Dependent Sympathetic Sprouting

  • $215,000/year (direct cost)
  • PI: Jun-Ming Zhang, MSc, MD
  • Agency: NIH/NINDS
  • Type: R01 (NS045594, Year 6-10), Period: May 1, 2004 – April 30, 2015

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

  • $289,742/year (total $2.0M including direct and indirect cost)
  • PI: Jun-Ming Zhang, MSc, MD
  • Agency: NIH
  • Type: R01 (NS055860, Year 6-10), Period: 12/15/ 2007 – 01/31/2018.

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.