Articles: hyperalgesia.
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The primary afferent nociceptor was used as a model system to study mechanisms of pain induced by chronic opioid administration. Repeated intradermal injection of the selective mu-opioid receptor (MOR) agonist DAMGO induced mechanical hyperalgesia and marked prolongation of prostaglandin E2 (PGE2) hyperalgesia, a key feature of hyperalgesic priming. ⋯ These studies demonstrate a novel form of hyperalgesic priming induced by repeated administration of an agonist at the Gi-protein-coupled MOR to the peripheral terminal of the nociceptor. Significance statement: The current study demonstrates the molecular mechanisms involved in the sensitization of nociceptors produced by repeated activation of mu-opioid receptors and contributes to our understanding of the painful condition observed in patients submitted to chronic use of opioids.
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The mechanisms underlying cyclin-dependent kinase 5 (Cdk5)-mediated thermal hyperalgesia induced by inflammation remain poorly understood. In the present study, we examined thermal hyperalgesia provoked by peripheral injection of complete Freund׳s adjuvant (CFA) to test for Cdk5 signaling in the spinal dorsal horns of rats through the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway, which is known to function in mediating inflammatory pain. ⋯ Cdk5, an upstream regulator of p38 and TNF-a, mediates CFA-induced thermal hyperalgesia. As such, pharmacological blocking of the generation of p-p38 mediated by Cdk5 may present a novel approach for diminishing inflammatory pain. This article is part of a Special Issue entitled SI: Spinal cord injury.
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Observational Study
The effects of electroacupuncture on analgesia and peripheral sensory thresholds in patients with burn scar pain.
The aim of this study is to observe if the effects of electro-acupuncture (EA) on analgesia and peripheral sensory thresholds are transposable from the model of heat pain in volunteers to the clinical setting of burn scar pain. After severe burns, pathological burn scars (PPBS) may occur with excruciating pain that respond poorly to treatment and prevent patients from wearing their pressure garments, thereby leading to unesthetic and function-limiting scars. EA might be of greater benefit in terms of analgesia and functional recovery, should it interrupt this vicious circle by counteracting the peripheral hyperalgesia characterizing PPBS. ⋯ The fact that acupuncture did not correct the pain nor the nociceptive thresholds in this subgroup requires further investigation. We also observed a statistically and clinically relevant reduction in VAS for pruritus for all patients - even those from the subgroup of non-responders to pain - that is worth to be mentioned and requires further studies to be confirmed. This observational study is the first that confirms the effects of acupuncture on analgesia and nociceptive thresholds in the clinical setting of burn pain only for patients presenting with a burn-localized but not a generalized hyperalgesia.
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Int. Immunopharmacol. · Sep 2015
Inflammatory mediators involved in the paw edema and hyperalgesia induced by Batroxase, a metalloproteinase isolated from Bothrops atrox snake venom.
Snake venom metalloproteinases have been described as responsible for several inflammatory effects. In this study, we investigated the edema and hyperalgesia induced in rats by Batroxase, a P-I metalloproteinase from Bothrops atrox venom, along with possible inflammatory mediators involved in these responses. Batroxase or sterile saline was injected into rat paws and the edema and hyperalgesic effects were evaluated for 6h by using a plethysmometer and a Von Frey system, respectively. ⋯ However, Batroxase itself induced minor degranulation of RBL-2H3 mast cells in vitro. Additionally, the inflammatory responses did not seem to be related to prostaglandins, bradykinin or nitric oxide. Our results indicate a major involvement of histamine and leukotrienes in the edema and hyperalgesia induced by Batroxase, which could be related, at least in part, to mast cell degranulation.
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Sleep deprivation induces hyperalgesia. However, this pro-nociceptive effect is not reflected at the electrophysiological level, since sleep restricted subjects show amplitude reduction of Laser-evoked Potentials (LEP). We aimed to explore the contribution of habituation to this paradoxical LEP amplitude decline. ⋯ TSD induces hyperalgesia and results in attention-dependent enhanced habituation of the P2 component. Increased habituation may--to a substantial degree--explain the TSD-induced LEP-amplitude decline. For this article, a commentary is available at the Wiley Online Library.