PhD, The University of Texas Health Science Center at San Antonio
Neurobiology of Pain, Migraine, Neuropharmacology
Greg Dussor received his PhD in Pharmacology at The University of Texas Health Science Center in San Antonio in 2002. He studied under the mentorship of Drs. Chris Flores and Ken Hargreaves where he worked on the modulation of peripheral nociceptors in the trigeminal system by cholinergic receptors. Following his PhD studies, he did postdoctoral training from 2004-2007 in the laboratory of Dr. Ed McCleskey at the Vollum Institute on the campus of The Oregon Health & Science University in Portland. There, he worked on biophysical properties of acid-sensing ion channels (ASICs) and also characterized the ion channel expression on a population of sensory neurons that innervate the outer epidermis. In 2007, he joined the Faculty in the Department of Pharmacology at the University of Arizona in Tucson. While in Arizona, he shifted the focus of his laboratory to understanding the pathophysiology contributing to chronic headache disorders such as migraine. He remained on faculty there until joining the School of Behavioral and Brain Sciences in 2014. Greg was a recipient of a Future Leaders in Pain Research Award from the American Pain Society, he has received funding from the NIH, the American Pain Society, the National Headache Foundation, and the Migraine Research Foundation, he is on the Editorial Board for the journal PAIN, and he regularly serves as a study section member at NIH/CSR.
Migraine has traditionally been thought of as a vascular disorder. However, it has become clearer in recent years that vascular changes cannot account for the pathophysiology of migraine and that maladaptive changes in the nervous system are more likely to contribute to this disorder. The exact changes in the nervous system contributing to migraine are not yet fully understood. The recent Global Burden of Disease Study by The Lancet (Vos et al 2012) found that migraine is the 3rd most prevalent disease in the world. Given this prevalence and the likely changes in the nervous system that lead to migraine, this makes migraine by far the most common neurological disorder. Unfortunately, less than 50% of migraine patients achieve adequate relief from currently available therapeutics. Studies in our laboratory are focused on mechanisms that mediate the pain of migraine. Using both in vitro and in vivo studies, we are focused on mechanisms leading to activation/sensitization of nociceptors innervating the cranial meninges including the potential contribution of non-neuronal cells (fibroblasts) to these processes. We are also interested in neuroplasticity that occurs across the central projections of these neurons the trigeminal nucleus caudalis and how this may contribute to lowered thresholds for headaches in migraine patients.
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.