Grant: CIHR Fellowship

Chronic pain is a public health concern affecting over 20% of the world population, leading to physical and emotional distress, and to the loss of patients' autonomy and quality of life. Over the past decades, tremendous efforts have been made in the discovery of new pain targets and in the development of novel analgesics. Yet, the number of pharmacological treatment options for chronic pain management remains limited, and too often ineffective. In light of the ongoing opioid crisis, the need for novel pain medication is particularly urgent. Given the recurrent failures in drug development, we clearly need to delve deeper into the pathophysiology of chronic pain, to better understand the transition from acute to chronic pain and to identify new therapeutic targets. Our previous studies identified a population of immune cells infiltrating the peripheral nervous system responsible for the development of chronic pain. The aim of this project is therefore 1) to investigate the molecular and cellular mechanisms involved in the transition from acute pain to chronic pain within the immune system in order to 2) identify new therapeutic targets in the treatment of pain. The study is based on an animal model of neuropathic pain through which we wish to identify the molecular dynamics within different immune populations in the transition from acute pain to chronic neuropathic pain. We will also identify the impact of different peripheral immune populations on the molecular deregulation of sensory neurons following nerve injury. Finally, we wish to identify specifically the cell populations responsible for nervous hyperexcitability by inhibiting each of them and by measuring their impact on the development of chronic pain using behavioral pain tests.