Abstract
(1) Background: Acupuncture (AP) is a safe and effective analgesic therapy. Understanding how fine needles trigger biological signals can help us optimize needling manipulation to improve its efficiency. Adenosine accumulation in treated acupoints is a vital related event. Here, we hypothesized that extracellular ATP (eATP) mobilization preceded adenosine accumulation, which involved local activation of mechanosensitive channels, especially TRPV4 protein. (2) Methods: AP was applied at the injured-side Zusanli acupoint (ST36) of acute ankle arthritis rats. Pain thresholds were assessed in injured-side hindpaws. eATP in microdialysate from the acupoints was determined by luminescence assay. (3) Results: AP analgesic effect was significantly suppressed by pre-injection of GdCl3 or ruthenium red in ST36, the wide-spectrum inhibitors of mechanosensitive channels, or by HC067047, a specific antagonist of TRPV4 channels. Microdialysate determination revealed a needling-induced transient eATP accumulation that was significantly decreased by pre-injection of HC067047. Additionally, preventing eATP hydrolysis by pre-injection of ARL67156, a non-specific inhibitor of ecto-ATPases, led to the increase in eATP levels and the abolishment of AP analgesic effect. (4) Conclusions: These observations indicate that needling-induced transient accumulation of eATP, due to the activation of mechanosensitive TRPV4 channels and the activities of ecto-ATPases, is involved in the trigger mechanism of AP analgesia.
Highlights
As a traditional Chinese medicine, acupuncture (AP) has been gradually accepted worldwide
We showed that subcutaneous mast cells were present at a higher density in acupoints and their degranulation was one of the triggering signals in the mechanism of needling acupuncture analgesia [3]
Our previous in vitro work demonstrated that the transient receptor potential vanilloid 4 channels were expressed on the human mast cell line HMC-1, together with mechanosensitive TRPV2 [7] and chloride [8] channels
Summary
As a traditional Chinese medicine, acupuncture (AP) has been gradually accepted worldwide. To date, considerable basic studies have been executed to explore the underlying mechanisms of AP analgesia [2], it is still not fully understood how the anti-nociceptive signals are initiated by fine needles at the acupoints. According to our previous work on rats, mechanical stimulation was the main physical stimulus applied on acupoints during manual AP [3]. We showed that subcutaneous mast cells were present at a higher density in acupoints and their degranulation was one of the triggering signals in the mechanism of needling acupuncture analgesia [3]. Our previous in vitro work demonstrated that the transient receptor potential vanilloid 4 channels were expressed on the human mast cell line HMC-1, together with mechanosensitive TRPV2 [7] and chloride [8] channels.
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