Interestingly, this latent, or secondary, injury develops over days and even weeks after the initial injury. It also appears to cause larger, more debilitating lesions in the spinal cord, said Randy Christensen, the study's lead author and a postdoctoral researcher in neuroscience at Ohio State University.
"Preventing over-stimulation caused by glutamate and TNFa together may be a viable strategy for therapeutic intervention after human spinal cord injury."
Receiving the initial brunt of the secondary trauma seem to be the neurons, or the cells in gray matter. As time passes, however, tissue in the white matter is also destroyed by secondary damage. Oligodendrocytes, the main cell type in white matter, begin to self-destruct during the secondary injury.
Oligodendrocytes protect the white matter's axons long, skinny tails attached to nerve cells that carry nerve cell messages throughout the body.
"These long, fragile extensions of nerve cells are probably very vulnerable," Christensen said.
The researchers presented their results Nov. 12 in New Orleans at the annual Society for Neuroscience meeting. Christensen conducted the study with Jacqueline Bresnahan, a professor of neuroscience at Ohio State, and Michael Beattie, the chair of Ohio State's neuroscience department.
The researchers injected glutamate, tumor necrosis factor-alpha (TNFa) or both molecules into the spinal cords of healthy, uninjured rats. Glutamate is a neurotransmitter, while TNFa is a potent cell stimulator its function includes stimulating the body's immune response after injury. Both are released in dangerously high concentrations at the site of a spinal cord injury.