A Dalhousie University scientist and his colleagues have discovered a “volume knob” for the brain when it tells the body to walk.
The finding reveals a new aspect of the complex neurological system that could one day improve treatment for spinal cord injuries and diseases like amyotrophic lateral sclerosis, said Dr. Robert Brownstone, a neurosurgeon and professor of anatomy and neurobiology.
It is already known that the brain relies on cells called motor neurons to translate messages like “walk” or “turn” into action.
“When we walk, our brain has better things to do than to think about which muscles to control,” Dr. Brownstone said Monday. “Those motor neurons can be getting the signals, but unless the volume is turned up, they’re not going to produce movement. Essentially what we’ve found here is kind of like a volume knob within the spinal cord.”
Dr. Brownstone and colleagues Gareth Miles of the University of St. Andrews, who studied in the Dal lab, and Andrew Todd and Robert Hartley of the University of Glasgow in Scotland described the system of spinal interneurons they discovered. Their findings are outlined in the journal Proceedings of the National Academy of Sciences of the United States of America.
A few interneurons in the spinal cord act to amplify signals from the brain to many motor neurons.
Mr. Miles demonstrated that when these cells in mice are activated, the electrical output from the motor neurons, telling muscles to contract in response to chemical signals from the brain, is much larger than when the cells are not activated.
Because the interneurons related to walking are located in the lower back, they’re typically unaffected by spinal cord injuries.
Many people working on repairing the spinal cord are seeking ways to grow severed nerve fibers across injury sites, Dr. Brownstone said. But the fibers need to know where to go and what to do.
He said discoveries like this one, supported by funding from the Canadian Institutes of Health Research, offer hope that re-establishing even a small connection across an injury site could be enough to get messages from the brain to the rest of the body when these amplifiers are manipulated.
Some people with spinal cord injuries experience spasms, suggesting the signal amplifiers might be set too high, Dr. Brownstone said.
Amyotrophic lateral sclerosis, or Lou Gehrig’s disease, kills motor neurons in the spinal cord, gradually robbing a person of control of their body.
“If you have fewer of them they have to work harder,” Dr. Brownstone said. “Maybe we can just adjust the volume knob and make things a little easier.”
The next stages of research will try to draw a more complete picture of what other actions are affected by the amplification effect of the interneurons and examine the chemical receptors on the cells to determine what drugs might be used to manipulate them, he said.
Dr. Brownstone wouldn’t speculate when such treatments might be possible for people with spinal cord injuries or neurological disease, though he said collaborations like this one, with experts in Glasgow, help speed the process.
“Progress is much quicker now than it was 10 or 15 years ago,” he said. “But the last thing we want to do is move too quickly.”
By John Gillis