Molecular and cellular mechanisms promoting chronic pain development

One in four Canadians over the age of 15 suffers from chronic pain, a condition that is a major risk factor for anxiety and depression. Our understanding of the molecular mechanisms involved is incomplete, and there is a woeful lack of efficacious treatments, with less than half of all people suffering from chronic pain reporting any control of their pain. Moreover, although most people suffering from chronic pain are women and other people with ovaries, preclinical studies have almost exclusively used male rodent models (>80%), resulting in a major gap in our understanding. Neuroimaging studies of people with chronic pain provide an opportunity to employ reverse translational strategies to test hypotheses of pain chronification. Repeatedly, neuroimaging studies have identified structural and functional changes to multiple regions of the emotion-pain brain network, including the anterior cingulate cortex (ACC), nucleus accumbens (NAc), and amygdala, in people suffering from chronic pain. Accordingly, numerous studies of analogous brain regions in rodent models have also revealed changes in neuronal excitability and structure. Within this network, neuroplasticity of the rodent ACC has emerged as a critical step for chronic pain development. This talk will combine behavioural, molecular, and bioinformatic approaches to investigate neuroplastic changes within the cingulate cortex in mouse models of chronic pain. A major focus will be on glial-neuronal interactions, and the critical role astrocyte-neuronal metabolic coupling plays in pain-induced neuroplasticity. Sex differences will be highlighted, and mechanisms promoting pain chronification will be covered.

Hybrid Zoom link: https://utoronto.zoom.us/j/84917442572

Passcode: 786860

To request an individual meeting with the speaker, please contact Maithe Arruda-Carvalho (m.arrudacarvalho@utoronto.ca).

Visit https://www.takeharalab.com/bbseminar for further information.