Printed Poster | Session 2

012 – Dissociating sensory from motor: Temporal assessment of pain in experimental autoimmune encephalomyelitis

Julia Segal (1) – Courtney Bannerman (1) – Jaqueline Silva (1, 2) – Ian Gilron (1, 2, 3) – Nader Ghasemlou (1, 2, 3)
Departments of Biomedical & Molecular Sciences (1) – Departments of Anesthesiology & Perioperative Medicine (2) – Centre for Neuroscience Studies, Queen’s University, Kingston, Ontario, Canada (3)

Multiple sclerosis (MS) is an autoimmune disease of the nervous system that affects over 2.5 million people worldwide. While its root cause is unknown, MS is thought to be initiated by a CD4+ T cell-mediated response that attacks myelin sheaths surrounding axons, leading to significant motor, sensory, and cognitive deficits, as well as autonomic dysfunction, fatigue, and pain. Experimental autoimmune encephalomyelitis (EAE) is a commonly used murine model of MS that recapitulates many of these symptoms. Although up to 80% of MS patients experience chronic pain, the EAE model causes hindlimb paralysis, which prevents meaningful nociceptive measurements that rely on stimulus-evoked motor responses. We therefore sought to adapt the EAE model to allow for the phenotyping of pain during the full course of disease. Using a dose-response strategy, our findings suggest that a lower dose of pertussis toxin than typically used in EAE reduces disease severity but amplifies mechanical and cold pain responses. Hallmarks of disease pathology, such as demyelination, immune cell recruitment, cytokine expression, and glial activation, remain unaffected between EAE mice induced with low (100ng) and moderate (200ng) doses of pertussis toxin, while there are distinct differences in pain outcomes. Our work opens the way for the study of both pain outcomes and disease pathophysiology in this murine model of MS.