Narrow Results

It has been reported by Stein et al. that the immune system and peripheral opioid receptors are involved in the control of pain accompanying inflammation. Electroacupuncture (EA) is used to relieve various kinds of pain. However, little is known about the effect of electroacupuncture analgesia (EAA) during hyperalgesia elicited by inflammation. The aim of the present study was to compare (1) the individual variation of EAA, (2) the durability of EAA, and (3) the effect of naloxone on EAA between normal rats and rats subjected to acute inflammatory pain. Carrageenan was subcutaneously administered by intraplantar (i.pl.) injection of the left hind paw to induce a nociceptive response. Nociceptive thresholds were measured using the paw pressure threshold (PPT). Rats received EA at 3 Hz in the left anterior tibial muscles for 1 hour after carrageenan injection. Naloxone was administered by intraperitoneal (i.p.) or i.pl. injection just before EA. EAA was elicited in 15 of 29 normal rats. These rats were divided into responders and non-responders. EAA in the responder group was almost completely antagonized by i.p. injection of naloxone. In contrast, in all the rats with carrageenan-induced inflammation, EAA was elicited, lasted for at least 24 hours after carrageenan injection, and was dose-dependently antagonized by i.pl. injection, but not significantly by i.p. injection of naloxone. It seems likely that the EAA in the rats with carrageenan-induced inflammation differs from that in normal rats, and these findings suggest that peripheral opioid receptors are involved in EAA during inflammatory conditions.

Electroacupuncture (EA) is used to relieve various kinds of pain. However, the mechanistic basis of electroacupuncture analgesia (EAA) in inflammatory pain remains unclear. In the present study, we investigated whether endogenous peripheral corticotropin-releasing factor (CRF) or interleukin-1β (IL-1) participated in EAA during hyperalgesia elicited by carrageenan-induced inflammation. Carrageenan was subcutaneously administered by intraplantar (i.pl.) injection of the left hind paw to induce inflammation. Nociceptive thresholds were measured using the paw pressure threshold (PPT) (Randall Sellito Test). Rats received 3 Hz EA in the left anterior tibial muscles for 1 hour after carrageenan injection. The selective CRF antagonist, α-helical CRF, or the recombinant IL-1 receptor antagonist, IL-1ra, was administered by i.pl. injection of the inflamed paw or by intravenous (i.v.) injection 1 hour before EA. PPT decreased significantly 3 hours after carrageenan injection. This decrease persisted at least 24 hours after carrageenan injection. EA resulted in significant increases of PPT, moreover, PPT elevations lasted 24 hours after carrageenan injection. By contrast, PPT elevations produced by EA were dose-dependently antagonized by local i.pl. injection of α-helical CRF or IL-1ra. This PPT elevation was not influenced by i.v. injection of α-helical CRF or IL-1ra. These findings suggest that peripheral CRF or IL-1 participate in EAA during hyperalgesia. The release of CRF or IL-1 elicited by EA may trigger the release of opioid peptides within inflamed tissue which may activate peripheral opioid receptors and inhibit the pain.

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Recent studies effected by our Institute indicate that various forms of human arthritis express both immunohistochemically and biologically active nerve growth factor (NGF) in the ynovium. In the present study, we used a model of carrageenan-induced arthritis to further evaluate the effects of joint inflammation on NGF level. These studies showed that experimentally-induced arthritis in rats caused a significant increase in NGF in the perivascular area of the synovium. We also showed that injection into the synovium of purified NGF did not cause inflammation per se and that the destruction of peripheral sympathetic innervation significantly reduced both the inflammation and the level of NGF following carrageenan injection.