Kristen Sparrow • June 27, 2011
This is a study that tries to specify which opioid receptors are involved in electroacupuncture’s effectiveness in decreasing the Paw Pressure Threshold in rats. They use an irritant, carrageenan, which makes the joint hyperalgesic (more sensitive) and then measure how long it takes for the rat to pull away after pressure. The electroacupuncture effect lasts for many hours, so they injected the opiate antagonist at various times after the electroacupuncture.
Their findings suggest “that peripheral µ, d and ? receptors on peripheral nerve terminals are activated by EA, although there is a time difference among these activations.”
Involvement of peripheral opioid receptors in electroacupuncture analgesia for carrageenan-induced hyperalgesia.
Department of Clinical Acupuncture and Moxibustion, Meiji University of Integrative Medicine, Nantan-shi, Kyoto, Japan. email@example.com
Taguchi R, Taguchi T, Kitakoji H.
Acupuncture is widely used to relieve pain; however, the mechanism underlying electroacupuncture analgesia (EAA) during inflammatory pain is unclear. We investigated whether endogenous peripheral opioid receptors participated in EAA during hyperalgesia elicited by carrageenan-induced inflammation. Moreover, we investigated which subtype of opioid receptor was involved in EAA. Carrageenan was subcutaneously administered by intraplanter (i.pl.) injection into the left hind paw. Nociceptive thresholds were measured using the paw pressure threshold (PPT). Rats received 3Hz electroacupuncture (EA) for 1h after carrageenan injection. The nonselective peripheral opioid receptor antagonist, naloxone methiodide, was administered by i.pl. injection of the inflamed paw 5min before EA. Also, animals received i.pl. or intravenous (i.v.) injection of selective antagonists against µ(D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-ThrNH2, CTOP), d(naltrindole, NTI), or ? (nor-Binaltorphimine, nor-BNI) opioid receptors 1h before EA. PPT decreased significantly 3h after carrageenan injection. EA resulted in significant increases of PPT, moreover, PPT elevations persisted for 9h after carrageenan injection. PPT elevations produced by EA were antagonized by local i.pl. injection of naloxone methiodide at 3 and 5h after cessation of EA. NTI, nor-BNI and CTOP blocked EAA from immediately, 1h, and 3h after EA cessation, respectively. The EAA in the inflamed paw could not be blocked by i.v. injection of NTI, nor-BNI and CTOP. These findings suggest that peripheral µ, d and ? receptors on peripheral nerve terminals are activated by EA, although there is a time difference among these activations.
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