Study Finds Old Trauma Increases Susceptibility to Stress

A wound can leave a lasting mark — even after it heals. A new study published in the journal Current Biology found that traumatic experiences can subtly prime the body to overreact and make it more sensitive to stress, pain, and fear — long after the physical injury has disappeared.

These findings may help explain how early trauma or injury can set the stage for chronic pain conditions in which the nervous system remains hypersensitive even after the initial injury has fully healed.

Scientists at the University of Toronto Mississauga found that mice with a history of injury had a heightened response to the scent of a predator, an extremely stressful stimulus for rodents. These mice showed marked fear and developed long-term pain in both hind legs, including the one that had not been injured. Remarkably, the symptoms persisted for more than six months, long after the original wound had physically healed.

“Our brains are hardwired to protect ourselves — especially from threatening situations. But sometimes this defense system stays on, leaving us hypersensitive to stress or pain long after the threat has passed. Our study provides new insights into how traumatic experiences can affect the brain’s response to future challenges, and may pave the way for more effective treatments for chronic pain and anxiety disorders,”
said Dr. Lauren Martin, senior author of the study and an associate professor in the Department of Psychology at the University of Toronto.

The study’s first author, Jennette Baumbach, a graduate student in Martin’s lab, identified a key link between stress and long-term pain. She found that the stress hormone corticosterone interacts with a protein called TRPA1 — often called the “wasabi receptor” because it triggers the characteristic burning sensation — to heighten sensitivity to future threats. This signaling loop appears to keep the nervous system on alert for danger, causing mice to respond to the scent of a predator with heightened fear and renewed pain — despite the absence of new injury.

Notably, although both TRPA1 and stress hormones such as corticosterone were required for the heightened fear response, long-term pain was dependent only on stress signaling and not TRPA1. This suggests that fear and pain may be driven by separate but parallel biological mechanisms. Blocking the stress hormone corticosterone or inhibiting the TRPA1 receptor may reverse these heightened responses, opening the way to new therapeutic strategies for conditions such as chronic pain, post-traumatic stress disorder (PTSD), and other stress-related disorders.

“We’re looking at the brain and the central neural networks that control these behaviors,” says Dr. Martin. “By understanding how trauma reprograms the nervous system, we can begin to target the mechanisms that keep fear and pain locked in.”