An injury can leave a lasting imprint – even after healing. A new study in Current biology Notes that past injuries can calmly make the body to react excessively and be more sensitive to stress, pain and fear long after the disappearance of damage.
These results can help explain how early injuries or trauma can prepare the ground for chronic pain conditions, where the nervous system remains hypersensitive long after healing initial damage. Can prepare the ground for chronic pain conditions, where the nervous system remains hypersensitive long after healing initial damage.
Researchers from the University of Toronto Mississauga have discovered that mice with injury history responded more intensely to the smell of a predator, an extremely stressful event for mice. These mice have shown exaggerated fear and developed lasting pain in both hind legs, including the unless injured side. Surprisingly, the symptoms lasted more than six months, long after healing physically.
“Our brains are wired to protect us – especially against threatening situations. But sometimes this protection system remains on – leaving us too sensitive to stress or pain, even when the threat has been over. Our research gives us a new overview of how past injuries can shape the brain’s response to future challenges, and could open the door to better treatments for chronic pain and anxiety disorders. »»
Dr. Loren Martin, principal of the study and associate psychology professor, University of Toronto
The first author Jennet Baumbach, a student graduated from Dr. Martin’s laboratory, discovered a key link between stress and lasting pain. She found that the corticosterone stress hormone interacts with a protein called TRPA1 – often called “wasabi” receiver because it produces a distinctive burning sensation – to amplify sensitivity to future threats. This signaling loop seems to keep the nervous system initiated for danger, which makes mice respond to the smell of predators with increased fear and renewed pain, despite no new injury.
In particular, while TRPA1 and stress hormones like corticosterone were necessary for the response to exaggerated fear, lasting pain depended only on the signaling of stress, and not on TRPA1. This indicates that fear and pain can be motivated by separate but parallel biological mechanisms. The blocking of the corticosterone stress hormone or the inhibition of the TRPA1 receiver could reverse these increased responses, which opens the door to new therapeutic strategies for conditions such as chronic pain, SSPT and other stress -related disorders.
“We dissect the brain and central circuits that control these behaviors,” said Dr. Martin. “Understanding how the trauma reclassions the nervous system, we can start targeting the mechanisms that keep fear and pain enclosed in place. »»
