Bradley J Kerr
Dr Bradley J Kerr 
Adjunct Professor
Education:
BPhD-Neuroscience, University of London-King's College, London UK, 2001
BSc-Psychology, McGill University, 1996
Faculty:
Department of Anesthesiology and Pain Medicine, Adjunct Professor, Department of Pharmacology
Teaching: PMCOL 412, PMCOL 343
Contact Information:
Office: 533 HMRC
(☎) 780.492.3380
bjkerr@ualberta.ca
Awards/Operating Grants:
CIHR Project Grant, MS Canada Discovery Grant
Academic Activities:
My research group employs a variety of behavioural assays toassess pain and nociception. In addition, we also use a variety of behavioral assays to measure cognitive and affective changes that are affected in chronic pain conditions. Our aim is to understand the underlying mechanisms of chronic pain that accompany autoimmune diseases or following traumatic injury to the nervous system.
Research: Mechanisms of chronic pain after CNS injury or disease
Research Interests/Laboratory Techniques
The development of chronic pain after spinal cord injury or in diseases such as multiple sclerosis (MS) is a major clinical concern. The main focus of research in my laboratory is aimed at addressing the cellular mechanisms that generate neuropathic pain in these conditions. My research uses two primary animal models: a clinically relevant spinal contusion injury model and a mouse model of autoimmune demyelination that resembles MS, experimental autoimmune encephalomyelitis (EAE). My research aims to understand the specific pathways and cellular changes that arise in response to direct trauma or in chronic disease states that may promote the development of neuropathic pain. The lab employs a number of different strategies that include analysis at the cell and molecular levels, as well as systems level approaches to address this complex biological problem.
Selected Recent Publications2. Dworsky-Fried , Z., Faig, C.A., Vogel, H.A., Kerr, B.J.and Taylor, A.M.W. (2022) Centralamygdala inflammation drives pain hypersensitivity and attenuates morphine analgesia in experimental autoimmune encephalomyelitis. Pain 163(1): 49-61
3. Maguire, A.D., Bethea, J.R., Kerr, B.J. (2021) TNF in MS and its animal models:Implications for chronic pain in the disease. Frontiers in Neurology. Dec 6;12780876.
4. Hammod, B.P., Manek, R., Kerr, B.J., Macaulay, M.S. and Plemel, J.R. (2021) Regulation of microglia population dynamics throughout development, health, and disease. Glia. 69(12):2771-2797.
5. Dworsky-Fried , Z., Chadwick, C.I., Kerr, B.J.and Taylor, A.M.W. (2021) Multiple Sclerois and the endogenous opioid system. Frontiers in Neuroscience. Sept.17;15:741503
6. Yousuf, M.S., Samtleben, S., Lamothe, S., Friedman, T., Catuneanu, A., Thorburn, K., Desai, M., Tenorio, G., Schenk, G.J., Ballanyi, K., Kurata, H.T., Simmen, T. and Kerr, B.J. (2020). Endoplasmic reticulum stress in the dorsal root ganglia regulates large-conductance potassium channels and contributes to pain in a model of multiple
sclerosis. FASEB 34 (9): 12577-12598
7. Friedman, T. N., Yousuf, M.S., Catuneanu, A., Desai, M., Juzwik, C.A., Fournier, A.E., and Kerr, B.J. (2019) Profiling the microRNA signature of the peripheral sensory ganglia in experimental autoimmune encephalomyelitis (EAE). Journal of Neuroinflammaton. Nov 15;16(1):223. doi: 10.1186/s12974-019-1600-7.
8. Catuneanu, A., Paylor, J.W., Winship, I., Colbourne, F. and Kerr, B.J. (2019) Sex differences in central nervous system plasticity and pain in experimental autoimmune encephalomyelitis. Pain May;160(5):1037-1049. doi:10.1097/j.pain.0000000000001483.
9. Yousuf, M.S., Noh, M.C., Friedman, T.N., Zubkow, K., Johnson, J.C., Tenorio, G., Kurata, H.T., Smith, P.A. and Kerr, B.J. (2019) Sensory neurons of the dorsal root ganglia become hyperexcitable in a T-cell mediated MOG-EAE model of multiple
sclerosis. eNeuro. Apr 1;6(2):ENEURO.0024-19.2019. doi: 10.1523/ENEURO.0024-19.2019.
10. Mifflin KA, Yousuf MS, Thorburn KC, Huang J, Pérez-Muñoz ME, Tenorio G, Walter J, Ballanyi K, Drohomyrecky PC, Dunn SE and Kerr BJ. (2019) Voluntary wheel running reveals sex-specific nociceptive factors in murine experimental autoimmune
encephalomyelitis. Pain 160(4):870-881