Lecturer Yasunori Takayama of Showa University and Professor Makoto Tominaga of the National Institute for Physiological Sciences, National Institutes of Natural Sciences, et al. ANO1) interaction was found to be involved.
TRPV1, which is expressed in the sensory nerves of the skin, becomes activated when it receives capsaicin, the main pungent component contained in chili peppers. TRPV1 is also involved in the burning pain you feel when you eat spicy food.
Additionally, ANO1, which is expressed in the same sensory nerves as TRPV1 and is activated by calcium, is known to intensify burning pain. TRPV1 is an ion channel that is permeable to calcium, so when calcium flows into cells through activated TRPV1 and activates ANO1, the burning pain you feel when you eat spicy food gets worse.
On the other hand, the interaction between TRPV1 and ANO1 in the burning pain (inflammatory pain) that occurs during inflammation is not clear, and this research group investigated this through electrophysiological and biochemical analyses.
During inflammation, TRPV1 is phosphorylated by an intracellular protein called protein kinase C (PKC), making it more likely to be activated than normal. As a result, phosphorylated TRPV1 is slightly activated by low concentrations of capsaicin, which would not activate normal non-phosphorylated TRPV37, or by heat stimulation at a core body temperature of around 1°C.
However, it was found that even through this weak activation of TRPV1, ANO1 was still strongly activated. This suggests that the interaction between phosphorylated TRPV1 and ANO1, which is induced even by sensory stimuli that do not normally cause pain, is important for inflammatory pain.
This study shows that inhibiting the interaction between phosphorylated TRPV1 and ANO1 may be effective in suppressing inflammatory pain, and is expected to lead to a concept for the development of new analgesics.