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Dying nerves cause even more harm after spinal cord injury

te and TNFa work in tandem, essentially over-stimulating the tissue surrounding the original site of damage, causing the surrounding cells to "go into shock" and die.

In these experiments, the rats' spinal cords weren't injured, but the injections of glutamate and TNFa mimicked the effects of secondary injury. A group of control rats was injected with albumin, an innocuous protein, to make sure the injection itself hadn't caused the secondary injury.

The researchers found a delayed reaction . . . the axons near the injection site began breaking two days after injection. In related work, these researchers have found evidence of axons breaking up to fourteen weeks after an injury.

"While we're not sure why the axons begin to break so long after the initial injection, the cells meant to help the wound heal may get overly excited so much so that they destroy the axons," Christensen said. "Another possibility is that the protective oligodendrocytes take a couple of days to die, finally exposing the bare axons to damage.

"Preventing over-stimulation caused by glutamate and TNFa together may be a viable strategy for therapeutic intervention after human spinal cord injury."

While there was noticeable nerve cell loss and tissue damage in gray matter 90 minutes after injections, the axons were not affected at this point in time.

By day two after the injection, however, there were large lesions in the white matter surrounding the injection site as well as noticeable damage to the axons.

"The time course is pretty important, because in spinal cord injury, many of the cells don't die until long after the initial injury," Christensen said. "Dying neurons might release glutamate and TNFa, and that release eventually kills neighboring nerve cells, oligodendrocytes, and axons."


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Contact: Randy Christensen
Christensen.40@osu.edu
614-247-6869
Ohio State University
12-Nov-2003


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