Meet the Pain Management Online Certificate faculty; they are some of today’s top practitioners and educators.
Kyle Baumbauer, Ph.D.
One of the primary challenges for the central nervous system is decoding meaningful messages from the ongoing constant barrage of information arriving at its synapses. This challenge is even more difficult under circumstances of injury or inflammation when signals can be scrambled, amplified, or passed along inappropriate circuits. Multiple laboratories are exploring these processes and trying to unravel the mystery of how normal and adaptive pain shifts to a maladaptive chronic pain state. To explore these processes, research in my laboratory focuses on the neurons responsible for transmitting sensory information to the central nervous system; the primary afferents.
The lab uses different models to examine pain processing: inflammation, nerve injury, and spinal cord injury. Primary afferents are studied using ex vivo preparations that allow for comprehensive phenotyping of individual nerve fibers and determine how injury changes physiological properties of these neurons. Physiological characterizations of neurons are also coupled with gene expression profiling of individual afferents to examine shifts in expression patterns following injury. Genetic expression of channelrhoodopsin is also utilized to target specific populations of afferents to examine relative contributions to sensory processing. It is our hope that our results will lead to advances that aid in the treatment of pathological pain.
My primary interest lies in the understanding of gene x environment interactions on pain outcomes, with a particular focus on stress and injury/inflammation as environmental factors. Genetic factors have been shown to contribute significantly to variability in the response to painful stimuli. We are beginning to unravel the individual gene candidates and the families of genes that contribute to differences in pain responses. Using genetic correlation analysis with standard inbred strains of mice in addition to whole-genome quantitative trait locus (WTL) mapping with genetic reference populations as our most powerful tools, we are able to explore the genetic contribution to both somatic and visceral pain behaviors. Stress and inflammation can both modulate pain responses to various stimuli, and it is likely that different genes are involved in pain under normal conditions and the modulation of pain through environmental factors. Most recently, my research has focused on these issues as they relate to bowel pain after inflammation using animal models of Inflammatory Bowel Disease (IBD). The candidate genes identified in preclinical models can then be examined in clinical populations to determine whether these genes contribute to pain susceptibility in IBD patients. The goal is to further understand the mechanisms underlying persistent bowel pain and to use this knowledge to identify novel therapeutic targets to reduce pain and suffering in clinical populations.