The Nobel Prize in Physiology or Medicine 2021, awarded for the discoveries related to receptors for temperature and touch, is notably significant in recent scientific discourse. Among the receptors central to these findings is the Transient Receptor Potential Ankyrin 1 (TRPA1), a member of the TRP family channel. This channel is highly expressed in pain-sensing neurons found in the dorsal root ganglion and trigeminal ganglia.
TRPA1 is activated by a wide range of compounds, including natural substances like mustard oil and cinnamon. Additionally, it also responds to a myriad of endogenous products originating from oxidative stress and metabolism-derived substances. One such reactive oxygen species, hydrogen peroxide (H2O2), is known to stimulate TRPA1. Given that H2O2 appears rapidly at wound sites, it is suggested to play a role in wound or injury tissues.
Thus, we hypothesize that TRPA1 has a crucial role in the pain mechanism following an incision in the deep muscle tissue. Our previous research demonstrated that incised deep muscle tissue, rather than skin, primarily contributes to the genesis of non-evoked pain behavior after plantar incision in rats. We further established that TRPA1 ligands such as H2O2 are produced in wounds, and that injection of H2O2 into muscle, as opposed to skin, elicits significant nociceptive behavior through TRPA1. These findings underscore the potential contribution of TRPA1 to nociception caused by deep tissue incision.
In our recent work, we conducted several experiments and published multiple papers elucidating the role of TRPA1 in surgery-induced sensitization of muscle nociceptors. In the meeting, I am going to discuss the role of TRPA1 after surgery in deep muscle tissues, drawing on both our published and yet-to-be-published data.
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