Katharina Buczek
This means that the K710N mice represent a good middle-ground. While they felt less pain, they were still able to maintain body temperature and sense potentially harmful stimuli.
Additionally, TRPV1 is responsible for even more functions in the human body– for instance, protecting us from organ damage.
In the study, though, the researchers found that the K710N variant did not just retain these functions but actually enhanced some of TRPV1’s protective benefits. For instance, heart cells that had the variant were actually less likely to die following temporary oxygen deprivation.
Custom Chronic Pain Drug
Equipped with these findings, the researchers then decided to design a custom-made drug that yielded the same effect as the K710N mutation.
The drug is a peptide known as V1-cal. And when it was administered to the mice– either via infusion or injection– the mice experienced less chronic pain from nerve injury and reduced capsaicin sensitivity.
Plus, the drug was found to have little impact on body temperature regulation and heat sensation.
TRPV1 has been a target for pain treatments in past research. However, Gross claims that the new drug is more selective and results in fewer side effects.
“People have always used a direct approach, so they looked at ways to specifically activate or block the receptor. That’s been a challenge because activation of the receptor causes pain, while inactivation may cause unwanted changes in body temperature,” Gross detailed.
In their study, though, Gross and his team did not focus on directly activating or inactivating the pain receptor. Instead, the new drug modulates one specific region of the receptor– and in doing so, the side effects can be circumvented.
“We are able to avoid the side effects that have been plaguing drug discovery for TRPV1 for quite some time,” Gross said.
