Dr. Theodore Price, PhDAssociate Professor
University of Texas at Dallas
Title: Switching circuits: how differences in coding of acute and chronic pain may lead to better pain therapeutics
June 7th: 10 am EST, 9 am CST, 7 am PST.
About Theodore Price
Theodore (Ted) Price returned to the School of Behavioral and Brain Sciences at UT Dallas as an Associate Professor in 2014. He graduated from UTD in 1998 with a BS in Neuroscience where he worked with Dr. Alice O'Toole on human face perception.
He then received his PhD in 2003 from the University of Texas Health Science Center at San Antonio under the mentorship of Christopher Flores and Kenneth Hargreaves where he worked on cannabinoid pharmacology and pain.
He was then a postdoctoral fellow in the laboratory of Fernando Cervero at McGill University until 2007 where he developed the first studies on how local control of protein synthesis in neurons is involved in the development of chronic pain disorders
He was a faculty member of The University of Arizona School of Medicine from 2007-2014 where he further developed work on nervous system plasticity in relation to pain with funding from the National Institutes of Health (NIH)-, Rita Allen Foundation- and Migraine Research Foundation.
Dr. Price is the recipient of Young Investigator Awards from the American Pain Society and International Association for the Study of Pain, has published more than 50 peer-reviewed articles in international journals, serves as the pharmacology section editor for European Journal of Pain, and is on the editorial board for Pain, Molecular Pain and The European Journal of Neuroscience. He is also a regular reviewer for National Institutes of Health and American Pain Society study sections.
Pain Research in the Price Lab
Pain serves a vital teaching function because it instructs organisms to avoid harmful stimuli. Pain plasticity is likewise a key feature of complex nervous systems because it signals for an organism to protect an injured area until the healing process has run its course. While these pain amplification mechanisms frequently resolve following healing, they can persist manifesting as chronic pain conditions. Moreover, chronic pain conditions (e.g. migraine headache) can arise without any apparent precipitating stimulus. Unfortunately these chronic pain conditions are poorly treated by current therapies creating an enormous burden of suffering with an economic impact estimated to be greater than diabetes, heart disease and cancer, combined! Hence, there is a great need to better understand mechanisms driving chronic pain and tailored therapeutic approaches that can reverse this aberrant plasticity
Our laboratory is interested in the fundamental principles underlying pain plasticity. Our goal is to develop novel therapeutics based on these discoveries with the potential to either prevent the development of or permanently reverse chronic pain states. We focus on two major areas: 1) plasticity in peripheral nociceptive neurons following injury and, 2) plasticity in central nervous system circuits that results from persistent stimulation of peripheral nociceptors. We utilize molecular, biochemical, genetic, behavioral and electrophysiological techniques combined with an overarching interest in pharmacology and drug discovery to tackle this problem.
Melemedjian OK#, Mejia GL, Lepow TS, Zoph OK, Price TJ# (2014). Bidirectional regulation of P body formation mediated by eIF4F complex formation in sensory neurons. Neuroscience Letters. 563 169-174. #co-corresponding authors
Price TJ, Dussor G (2013). AMPK: An emerging target for modification of injury-induced pain plasticity. Neuroscience Letters. S0304-3940(13) 607-1.
Parker SS, Mandell EK, Hapak SM, Maskaykina IY, Kusne Y, Kim JY, Moy JK, St John P, Wilson JM, Gothard KM, Price TJ#, Ghosh S#. (2013) Competing molecular interactions of aPKC isoforms regulate neuronal polarity. Proceedings of the National Academy of Sciences USA. 110(35) 14450-5. #co-corresponding authors.