New paper: Central amygdala inflammation drives pain in an animal model of multiple sclerosis

Read our new paper out now in the journal Pain.

Multiple sclerosis (MS) is an autoimmune disease characterized by chronic inflammation and demyelinating lesions within the central nervous system. Canada has one of the highest rates of MS in the world with 1 in 385 Canadians currently diagnosed with MS. Chronic pain is a highly prevalent symptom associated with MS, affecting 50-80% of patients over the course of their disease. Unfortunately, MS-associated chronic pain responds poorly to currently available analgesics, contributing to overall disease burden and reduced quality of life. The development of novel therapies for MS-associated pain is urgently needed to manage this disease.

Chronic pain is defined by multiple structural and functional changes within the central nervous system. While adaptations within nociceptive spinal and sensory circuits have rightfully received focused attention over the years, new research is beginning to explore how changes within affective circuitry can contribute to both the sensory and affective symptoms of autoimmune-associated pain. Patients with MS develop anatomical and functional changes in affective brain regions, particularly the amygdala. We also know that affective circuits can exacerbate the perception of pain, either through amplification of pain signals to the brain or by interfering with endogenous pain control. How the affective system changes in MS to exacerbate the sensory and affective symptoms of autoimmune-associated pain remains unclear.

Focal inflammation in the central amygdala impairs morphine analgesia in female, but not male mice

In this study, we demonstrated that a mouse model of MS results in functional changes in central amygdala activity. This altered activity correlated with increased pain behaviour and impaired morphine analgesia, specifically in females. This altered activity also coincided with robust inflammation within the central amygdala. Inducing inflammation focally within the central amygdala of healthy mice was sufficient to evoke pain behaviours seen in our chronic pain models. This suggests that inflammation within the central amygdala impairs nociceptive signaling and contributes to pain hypersensitivity in this model.

This project was lead by our graduate student, Zoë with help from then undergraduate students Holly and Christian. Zoë recorded a fantastic summary of this project for the journal. You can listen to it here.

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