A few weeks ago, Physicians Committee for Responsible Medicine called for an end to classes in spinal cord injuries that included specific techniques for creating animal models for such injuries. A recent discovery by a team at the University of Rochester Medical Center, however, underscores the important role that animal research plays in understanding complex changes in biological systems.
The short version is that researchers found that ATP — an energy source cells need to stay alive — plays an important role in causing damage to otherwise healthy cells after trauma in the spinal cord. After a spinal cord injury, ATP levels increase up to 100 times normal levels. Undamaged neurons essentially become over-stimulated and they die from metabolic stress.
According to a University of Rochester Medical Center press release,
The finding that ATP is a culprit in causing the devastating damage of spinal cord injury is unexpected. Doctors have known that initial trauma to the spinal cord is exacerbated by a cascade of molecular events over the first few hours that permanently worsen the paralysis for patients. But the finding that high levels of ATP kill healthy cells in nearby regions of the spinal cord that were otherwise uninjured is surprising and marks one of the first times that high levels of ATP have been identified as a cause of injury in the body.
Using an animal model of the disease opposed by PCRM — in this case in rats — the researchers created a compound that blocked the effect of ATP on neurons in the animals’ spinal cords after injury. The result? After six weeks the rats’ spinal cords had recovered most of their function and they were able to walk, run and climb as well as a healthy control group of rats.
Scientists finger surprise culprit in spinal cord injury. Press Release, University of Rochester Medical Center, July 28, 2004.
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