Resolving Chronic Pain The body’s own mechanism for dispersing the inflammatory reaction might lead to new treatments for chronic pain.
By Claudia Sommer and Frank Birklein - January 1, 2012
the-scientist.com
One of the interesting parts of the article:
Using an animal model of pain, investigators injected the paws of mice with formalin, which produces two phases of pain: an immediate reaction, relayed by the peripheral nerves; and a delayed-onset reaction, mediated by inflammation and by spinal cord neurons. 3The first phase is characterized by mice licking the injected foot for about five minutes after injection. Then, after a lag of 20–30 minutes, the second phase begins with another bout of foot licking. The researchers administered two different resolvin (Rv) molecules, RvD1 and RvE1, to test their ability to reduce this pain behavior, and found both molecules to be effective when injected either into the paw or directly into the spinal canal. They noted that RvE1 diminished swelling and reduced markers of the inflammatory response, and that, compared to either morphine or COX-2 inhibitors, a much lower dose of the resolvin effectively halted pain behavior. Interestingly, only the second phase of pain behavior—mediated by spinal cord mechanisms that are often associated with chronic pain—was attenuated, indicating that RvE1 and RvD1 were likely acting via a receptor known as ChemR23, a G protein–coupled receptor found on nociceptive neurons in the dorsal root ganglia and the dorsal horn of the spinal cord. These neurons also express the transient receptor potential vanilloid 1 (TRPV1), which is the receptor for the inflammation-producing irritant found in chili pepper, capsaicin. In living mice, RvE1 was able to block the pain induced by capsaicin.
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