Alexis Bavencoffe

We are studying new cellular targets to treat chronic pain, with an emphasis on patients with spinal cord injury (SCI) and chemotherapy-induced peripheral neuropathy (CIPN). After SCI or chemotherapy, primary nociceptors can switch from an electrically quiet into a hyperactive state enabling spontaneous discharge of action potentials (spontaneous activity, SA). This hyperactive state can enhance nocifensive reflexes and drive ongoing pain. Experimental approaches that block SA have already yielded promising results. We are using electrophysiological (patch-clamp) and behavioral approaches to identify signaling pathways (with an emphasis on cyclic AMP dependent pathways) recruited by circulating factors (e.g., proinflammatory cytokines) found in the plasma of patients that could elicit and maintain the nociceptor hyperactive state and chronic pain. The Bavencoffe Lab focuses in particular on the neuroimmune crosstalk mediated by proinflammatory cytokines between sensory neuron somata located within dorsal root ganglia (DRGs) and immune cells (e.g. macrophages, lymphocytes) leading to the nociceptor hyperactive state that promotes chronic neuropathic pain. We perform our investigations using preclinical rodent models of SCI and CIPN and test the translational potentials of our findings for future clinical applications on freshly dissociated human sensory neurons.