Our laboratory has recently published a study in the International Journal of Molecular Sciences that sheds new light on the mechanisms of pain hypersensitivity. Pain is often amplified by inflammatory molecules, among which bradykinin plays a key role. This molecule can heighten pain perception by acting on specialized ion channels in the nervous system, particularly the transient receptor potential vanilloid 1 (TRPV1) channel—a well-known target in chronic pain research.
In our experiments, we administered bradykinin directly into the spinal fluid of rats and observed a marked increase in pain sensitivity, both to heat and to mechanical touch. This hypersensitivity was further amplified when bradykinin was combined with N-oleoyldopamine (OLDA), a naturally occurring compound that also activates TRPV1. Interestingly, OLDA alone produced no effect, but in combination with bradykinin it significantly prolonged and intensified the pain response. Crucially, when animals were pretreated with a selective TRPV1 antagonist, the hypersensitivity was completely prevented.
These results provide direct evidence that spinal TRPV1 channels are central mediators of pain hypersensitivity triggered by bradykinin. They also demonstrate how endogenous molecules such as OLDA can interact with inflammatory pathways to enhance pain states. This discovery not only advances our understanding of spinal pain processing but also highlights TRPV1 as a promising therapeutic target for controlling excessive pain responses in chronic conditions.
By uncovering these mechanisms, our laboratory contributes to the development of more effective strategies for treating persistent pain—an area of pressing clinical need. This study reflects our ongoing commitment to translating fundamental neuroscience into potential therapeutic advances for patients suffering from chronic pain.
Uchytilova, E.; Spicarova, D.; Palecek, J. Hypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist. Int. J. Mol. Sci. 2021, 22, 3712. https://doi.org/10.3390/ijms22073712
