The current line of research in our lab is to use novel mouse models to investigate the role of toll-like receptor (TLR) – 4 on DRG nociceptive neurons vs. macrophages/microglia in chronic pain development. Specifically, we use this model to focus on the importance of cell-specific TLR4 deletion and reactivation during spared nerve injury and diabetic neuropathy, both models of neuropathic pain. Me and my lab has a long-term interest in neural circuit interactions within the nervous system. I have recently joined the faculty at UT Dallas and am currently working on breeding genetically-modified mice. We have access to extensive resources, such as the transgenic mouse lines, and an enriched research environment with major collaborative possibilities at both UTD and UTSW.
Check out Dr. Burton’s NIH Pain Consortium Symposium talk
Check out Dr. Burton’s Keystone Symposium short talk on TLR4
In addition to to TLR4, we have an interest in cannabinoid-signaling (CB1) in the context of analgesia. Understanding the complex network that regulates pain is fundamental to develop rational strategies to combat its growing prevalence and increased financial burden to the medical care system. An extensive literature has identified the importance of cannabinoid receptors and endocannibnoids in controlling pain. Despite this very large body of work, the neuronal-type responsible for cannabinoid-induced analgesia are not known. We aim to use an innovative genetic approach to elucidate the minimal circuitry capable of producing cannabinoid-induced analgesia in mice. This work will settle long-standing controversies in the cannabinoid analgesia area that will have an impact on the design of therapeutics targeting this system.
Check out some cleared sensory cortex using the sca/e technique.