Neuroplasticity underlies all types of experience-driven, long-term changes in the brain. Beyond mechanisms classically associated with memory, neuroplasticity represents fundamental processes that promote lasting changes in behaviour, such as nociceptive hypersensitivity. An important question remains: Do all neuroplasticity systems work the same way, or are there specific neuroplastic changes associated with specific experiences?
Neuronal plasticity is a fundamental, evolutionarily conserved process, that is essential for survival. Neurons however do not exist in a vacuum, and despite numerous advancements in our understanding of the molecular mechanisms involved in neuronal plasticity, several questions remain unanswered. Using nociceptive hypersensitivity as a model of experience-induced plasticity, our laboratory will identify the critical contributions of astrocyte-neuronal metabolic coupling in long term changes of neuronal function in nociceptive brain circuits.
Chronic pain is a major risk factor for anxiety and depression, and up to three quarters of individuals that suffer from chronic pain will develop comorbid anxiodepressive symptoms. Understanding how pain causes anxiety and depression will lead to advances in numerous aspects of basic and translational research into mental illness. Our research will identify fundamental mechanisms driving maladaptive neuroplasticity that promotes pain chronification and can cause long-term changes in mood.
The high comorbidity between chronic pain and anxiodepressive states suggests that persistent pain may alter neural function within brain regions that regulate mood. Indeed, neuroimaging studies of people with chronic pain show that numerous brain regions involved in emotion, which we term the emotion-pain brain circuit, show altered activity and functional connectivity. It is believed that pain chronification involves functional reorganization of these regions, promoting chronic pain and anxiodepressive states. Our studies bridge neuronal circuit function and gene expression profiles, with comprehensive behavioural analyses to determine the mechanisms involved in the development of chronic pain and comorbid anxiodepressive states.
Nearly 8 million Canadians over the age of 15 suffer from chronic pain, a rate that jumps to one in three for people over the age of 65. Notably, 67% of those individuals identify as women, yet most basic research on chronic pain has used male rodent models. As a result, there is a dearth of information regarding the fundamental mechanisms involved in chronic pain, and pain related anxiodepressive states, in women. Our research will thus ALWAYS include sex as a biological variable, and seeks to determine sexually dimorphic mechanisms of nociception and pain chronification.