AsianScientist (Apr. 16, 2015) – The sensation of pain via the transient receptor potential cation channel vanilloid 1 (TRPV1) is amplified by the activation of anoctamin 1 (ANO1), according to a study published in the Proceedings of the National Academy of Sciences.
TRPV1 is well-known as the pain receptor activated by capsaicin, an irritant found in chilli peppers. While hot water also activates TRPV1, capsaicin is a stronger stimulus. Because TRPV1 is a non-selective cation channel, it is believed that the influx of sodium ions (Na+) through TRPV1 pore causes depolarization, leading to the action potential generation.
In the present study, researchers have found a pain-enhancing mechanism that relies on calcium (Ca2+) rather than sodium ions. A team of researchers led by Dr. Makoto Tominaga from the National Institute for Physiological Sciences (NIPS) found that Ca2+ influx via TRPV1 activates ANO1, causing an efflux of chloride ions (Cl– via ANO1 which in turn generates the action potential.
In addition, Tominaga and colleagues found that the functional interaction between TRPV1 and ANO1 is based on their physical binding, indicating that Ca2+ ions work in the nanodomain within 20 nm. Furthermore, the research group observed that pain-related licking behaviors in mouse hind paws treated with capsaicin were inhibited by an ANO1 blocker.
The article can be found at: Takayama et al. (2015) Pain-enhancing Mechanism Through Interaction Between TRPV1 And Anoctamin 1 In Sensory Neurons.
Source: National Institutes of National Sciences.
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