A researcher at the University of Ottawa has identified a group of spinal neurons that play a major role in recovering mobility following a serious spinal cord injury. The study, led by Tuan Bui, Assistant Professor in the Department of Biology and researcher at the University of Ottawa’s Brain and Mind Research Institute, has been published in the life sciences journal eLife.
About 86,000 Canadians are currently living with spinal cord injuries, which occur when the spinal cord or nerves at the end of the spinal canal are damaged by trauma, illness, infection or inflammation. The impact of spinal cord injuries can be devastating, with effects ranging from full paralysis to partial paralysis and loss of sensation and mobility.
“Currently, there are no effective treatment strategies for those who have suffered serious spinal cord injuries,” explains Bui. “People who have lost the ability to walk face long periods of physical rehabilitation with only modest recovery, if any at all. Our goal was to identify neurons within the spinal cord that could promote recovery of locomotion following spinal cord injury, so that we could develop treatment strategies with better outcomes.”
While working with Nicolas Stifani in the lab of renowned neuroscientist Dr. Rob Brownstone at Dalhousie University (now at University College London), Bui and his colleagues identified a group of spinal neurons, named dI3 interneurons, which in animal models play a major role in the ability to recover mobility following a serious spinal cord injury. This is the first population of spinal neurons to be identified as crucial to the spinal cord’s ability to recover locomotion.
Mice that have lost the ability to move their hind limbs following spinal cord injuries can be trained to walk again on a treadmill. As the impaired hind limbs interact with the treadmill, the sensation of walking sends a signal to the spinal cord. This signal retrains the spinal cord to control the hind limb muscles to walk again. Bui and his colleagues found that while normal mice could be trained to walk on a treadmill following spinal cord injury, mice in which dI3 interneurons were silenced were unable to do so. These results suggest that the dI3 interneurons play an important role in converting sensation from the impaired hind limbs into a training signal for the spinal cord.
The team’s findings open new avenues for the treatment of spinal cord injuries. Bui is now looking to better understand how dI3 interneurons work to reconfigure the spinal cord to recover mobility following spinal cord injury, and whether dI3 interneurons are also present in humans.
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