Wright State researchers join a handful of select international teams to investigate spinal cord injury in a new grant program from the National Institute of Neurological Disorders and Stroke. Robert E.W. Fyffe, Ph.D., director of the new Center for Brain Research and professor of anatomy, will be the principal investigator for the $1.46M grant. The five-year grant is a collaboration between Wright State University School of Medicine and Queen's University, Kingston, Ontario, Canada.
"Traumatic spinal cord injury currently affects approximately 250,000 Americans, but there are so many unknowns when it comes to spinal cord injury," explains Fyffe. "Until we know what is happening at the cellular level, we will not be able to target appropriate treatments." To provide essential information the research team will examine the structure and function of interneurons in the uninjured spinal cord.
Interneurons are found in the gray matter of the spinal cord. There are many different classes of interneurons, and researchers believe the diversity is functionally meaningful but not yet understood.
Fyffe's team will examine the cellular properties of interneurons while a team under the direction of Kenneth Rose, Ph.D., in Canada, will develop computer models based on anatomical and neurochemical data from Fyffe's laboratory.
No one knows exactly how interneurons work or what specific chemicals they need to function. It appears that interneurons temper, or modulate, the activity of motoneurons which control muscle contraction in a coordinated way by sending electrical signals to particular muscles. Motoneuron activity depends on signals from the brain and on sensory feedback signals from receptors throughout the body. Assisting all of these message systems are interneurons, which are prolific nerve cells that interconnect the sensory feedback systems, the commands from the brain, and the motoneurons. In spinal cord injury, paralysis is caused because the descending pathways to the spinal cord are damaged. However, the circuitry of the sensory cells and motoneurons and interneurons remains intact, but unable to receive electrical messages from the brain. Because interneurons are so well connected, they likely contribute to the mechanisms that cause paraplegics and quadriplegics to develop muscle spasticity and therefore they may provide key clues about ways to minimize damage from a spinal cord injury, says Fyffe.