Spinal mechanisms of chronic pain: moving from targets in rodent models towards treatments for humans.

Pause-conférence | Pr Michael Hildebrand (Ottawa)

Le Pr Michael Hildebrand, professeur à la Carleton University, sera l’invité du Pr Said Kourrich, membre régulier du CERMO-FC, le Jeudi 14 novembre à 12h00 au SB-1115.

En savoir plus sur les recherches du Pr Hildebrand (anglais).

Pr Michael Hildebrand, a professor at Carleton University, will be the guest of Pr Said Kourrich, a regular member of CERMO-FC, on Thursday November 14th at 12:00 in SB-1115.

Learn more about Pr Hildebrand’s research.

Summary: Chronic pain represents a health crisis in Canada, with high prevalence and limited treatment options that are both safe and effective. The spinal dorsal horn is a key site of neuronal pathology in chronic pain states. We have discovered that in the nerve-injury rodent model of neuropathic pain, BDNF-mediated loss of inhibition (disinhibition) gates potentiation of excitatory NMDA receptors (NMDARs) at superficial dorsal horn synapses. However, the molecular linker between disinhibition and facilitated excitation remains unknown. In addition, there is a translational chasm between mechanistic studies in rodent models of pain and new treatments that work for humans. To bridge this translational divide, we have developed a human tissue preclinical model of pathological pain. By combining human and rat ex vivo BDNF models with a rodent in vivo model of inflammatory pain, we are investigating spinal mechanisms of pathological pain across species. We have found that the loss of a phosphatase associated with NMDARs, STEP₆₁, mediates the pathological coupling of disinhibition to NMDAR potentiation in both rats and humans. We have therefore discovered a conserved molecular mechanism that may inform the rational development of more effective treatment strategies for chronic pain.

Biography: Dr. Michael Hildebrand completed his PhD in cellular neuroscience in Terry Snutch’s lab at UBC. Using patch-clamp electrophysiological techniques, he characterized how the regulation of voltage-gated calcium channels impacts neuronal excitability. Following this, Dr. Hildebrand pursued an industrial R&D fellowship at Zalicus Pharmaceuticals in Vancouver, where he developed an ex vivo spinal cord recording assay for Zalicus’ preclinical pain research program. To further expand his expertise in spinal pain processing, Dr. Hildebrand then completed a postdoctoral fellowship in Mike Salter’s lab at Sick Kids Hospital in Toronto. In the Salter lab, Dr. Hildebrand investigated how the differential expression and regulation of synaptic NMDA receptors contributes to both physiological and pathological mechanisms of pain. Dr. Hildebrand is now leading his own pain research program as an Associate Professor at Carleton University, where his team is studying both acute and chronic pain processing using animal and human tissue models.

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