Project 465143
Investigating the role of molecular and functional plasticity within the brain emotion-pain circuit in the development of chronic pain.
Investigating the role of molecular and functional plasticity within the brain emotion-pain circuit in the development of chronic pain.
Project Information
| Study Type: | Unclear |
| Research Theme: | Biomedical |
Institution & Funding
| Principal Investigator(s): | Descalzi, Giannina |
| Institution: | University of Guelph |
| CIHR Institute: | Neurosciences, Mental Health and Addiction |
| Program: | |
| Peer Review Committee: | Behavioural Sciences - A: Neurobiological Basis of Behavioural Processes |
| Competition Year: | 2022 |
| Term: | 1 yr 0 mth |
Abstract Summary
One in four Canadians over the age of 15 suffer from chronic pain, a rate that jumps to one in three in Canadians over the age of 65. Understanding of the basic mechanisms involved in the transition from acute to chronic pain will help generate new treatments. Brain imaging studies of people with chronic pain show changes in the activity of multiple brain regions implicated in emotion, a network named the emotion-pain circuit. These regions are collectively activated by painful experiences and are involved in the emotional aspect of pain. Studies using mouse models have shown that a type of brain cell, the neuron, undergoes many changes in response to chronic pain, including increases in its activity and signaling to other brain regions in the emotion-pain circuit. Despite this progress however, we still do not fully understand how pain causes these changes to neurons. Recent work has shown that another brain cell, the astrocyte, can also affect neuronal activity, and we recently showed that astrocytes and neurons need to communicate for learning induced changes in the function of neurons. However, whether chronic pain increases communication between astrocytes and neurons in the emotion-pain circuit is unknown. The proposed research will use a mouse model to determine how astrocytes affect neurons during development of chronic pain. Specifically, we will utilize genetic tools to reduce the communication between astrocytes and neurons in the brain to determine if the development of chronic pain can be prevented. We will employ magnetic resonance imaging (MRI) to scan the brains of mice and determine if nerve injury causes changes in the activity and communication between brain regions in the emotion-pain circuit, and if communication between astrocytes and neurons is required. These findings will provide a leap forward in our understanding of the molecular machinery involved in the development of chronic pain, and will propel research into better treatments.
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