Pain, with an emphasis on chronic headache disorders such as migraine.
Dr. Greg Dussor’s research focus is on uncovering pathological mechanisms and therapeutic targets for migraine headache. Since the most likely mechanism contributing to migraine pain is activation of peripheral nociceptive signaling from the meninges, experiments in the Dussor laboratory have focused on identifying cellular mechanisms of dural afferent activation/sensitization as well as understanding plasticity at the central terminals of these neurons. Published manuscripts resulting from this work have identified targets within the afferent nociceptive system that innervates the meninges, including acid-sensing ion channels, several TRP channels, and IL-6 signaling mechanisms. They have also identified non neuronal cells (fibroblasts) as potential contributors to afferent signaling from the meninges. Dr. Dussor has moderated two webinars on migraine hosted by the Pain Research Forum and has been interviewed on KERA’s Think! program. He also is a recipient of a “Future Leaders in Pain Research” award from the American Pain Society, serves as Associate Editor for the journal PAIN, and regularly participates in several NIH study section panels. He has received funding for his work from the NIH, the Migraine Research Foundation, the National Headache Foundation, and several industry sources. Dr. Dussor earned his bachelor’s degree from the University of Alabama and his PhD from the University of Texas Health Science Center in San Antonio.
Wei X, Melemedjian OK, Ahn DD, Weinstein N, Dussor G. (2014). Dural fibroblasts play a potential role in headache pathophysiology. Pain. Doi: 10.1016/j.pain.2014.03.013
Yan J, Wei X, Bischoff C, Edelmayer RM, Dussor G. (2013). pH-evoked dural afferent signaling is mediated by ASIC3 and is sensitized by mast-cell mediators. Headache, 53(8):1250-1261.
Yan J, Melemedjian OK, Price TJ, Dussor G. (2012). Sensitization of dural afferents underlies migraine-related behavior following meningeal application of interleukin-6 (IL-6). Mol Pain, Jan 24; 8:6.