A new pathway to treat pain from spinal cord injury

Riyi Shi (Photo/Andrew Hancock)

11/23/2015 |

New research on a toxin released by the body in response to spinal cord injuries could point to a new route for treating pain in people with such injuries, according to Riyi Shi, professor of neuroscience and biomedical engineering in Purdue Veterinary Medicine’s Department of Basic Medical Sciences and the Weldon School of Biomedical Engineering. The research found that a neurotoxin called acrolein, which is produced within the body after nerve cells are damaged, increases pain by causing a proliferation of channels containing pain sensors, and this hypersensitivity also extends to peripheral nerves in the limbs far from the injury site.

Shi says the proliferation of channels increases the number of binding sites for the toxin, evidently worsening pain and causing a cell’s genetic material to signal for over-production of pain receptors called TRPA1, or transient receptor potential ankyrin, which results in hypersensitivity to pain in both the spinal cord and the limbs. “The data suggest that acrolein has the capability to cause widespread sensory hypersensitivity and likely plays an essential role in neuropathic pain extending beyond the location of the original injury,” Shi says.

Revelations that acrolein worsens pain in peripheral nerves points to a potential new treatment approach, perhaps by stimulating nerve endings in extremities, according to Shi. Another potential treatment strategy is reducing the concentration of acrolein using the drug hydralazine, which has been approved by the U.S. Food and Drug Administration for hypertension.

Research findings are detailed in a paper recently published online in the Journal of Neurochemistry. The paper was authored by graduate students Jonghyuck Park, Lingxing Zheng, Glen Acosta, Sasha Vega-Alvarez and Breanne Muratori; former postdoctoral researcher Zhe Chen who worked with surgeon Peng Cao at Shanghai Jiao-Tong University in China; and Shi.

– Emil Venere
See original news release at bit.ly/1QRyQSK