Dr. Michael Hildebrand completed his PhD in Molecular and Cellular Neuroscience in 2008 at the University of British Columbia. He did an industrial postdoctoral fellowship at Zalicus Pharmaceuticals in Vancouver from 2008 to 2010 followed by an academic postdoctoral fellowship at the Sick Kids Hospital in Toronto from 2010 to 2013. Dr. Hildebrand began his research lab at Carleton University in 2013. He's also an avid runner and loves candy!
Eligible to supervise at the undergraduate and graduate level.
The Hildebrand Lab investigates spinal mechanisms of pain processing. They use a combination of molecular, pharmacological, electrophysiological, and behavioural approaches to identify the molecular pathways that regulate pain sensation in both acute and chronic pain states. The goals of the lab include:
Mahmoud, H., Martin, N., Hildebrand, M.E. (2020) Conserved contributions of NMDA receptor subtypes to synaptic responses in lamina II spinal neurons across early postnatal development. Molecular Brain 13: 31.
Dedek A, Xu J, Kandegedara C, Lorenzo LE, Godin AG, De Konick Y, Lombroso PJ, Tai EC, Hildebrand ME. (2019) Loss of STEP61 couples disinhibition to N-methyl-D-aspartate receptop potentiation in rodent and human spinal pain processing. Brain, Volume 142, Issue 6, Pages 1535-1546.
Hildebrand ME, Xu J, Dedek A, Li Y, Sengar AS, Beggs S, Lombroso PJ, Salter MW. (2016) Potentiation of synaptic GluN2B NMDAR currents by Fyn Kinase is gated through BDNF-mediated disinhibition in spinal pain processing. Cell Reports, 17(10):2753-65.
Hildebrand ME, Pitcher GM, Harding EK, Li H, Beggs S, Salter MW. (2014) Dominant GluN2B and GluN2D-mediated synaptic responses in the adult spinal cord. Scientific Reports 4: 4094 (12 pages)
Bourinet E, Altier C, Hildebrand ME, Trang T, Slater MW, Zamponi GW. (2014) Calcium permeable ion channels in pain signalling. Physiological Reviews 94(1): 81-140.
