• Emily K Davies, Yvonne Boyle, Boris A Chizh, Bridget M Lumb, and Joanna C Murrell.
• School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK.
• Pain. 2011 Dec 1;152(12):2844-51.

AbstractCutaneous inflammation induced by ultraviolet (UV) irradiation in the UV-B range has received significant recent interest as a translational inflammatory pain model. Changes in thermal and mechanical sensitivities in the area of primary hyperalgesia are well documented in both the rat and human UV-B models, but the occurrence of secondary mechanical hyperalgesia is controversial. We investigated the occurrence of secondary mechanical hyperalgesia in the rat UV-B model. Additionally, we investigated whether secondary hyperalgesia was enhanced by heat rekindling of UV-B-irradiated skin as a new rat inflammatory model of sensitisation with an enhanced central contribution. UV-B irradiation (1000 mJ/cm(2)) induced significant secondary mechanical hyperalgesia and allodynia that peaked at 48 h. Heat rekindling (45 °C stimulus for 5 min) of UV-B-irradiated skin at 24h further enhanced and prolonged this secondary mechanical hyperalgesia and allodynia, with a peak at 72 h. Heat rekindling also induced a significant mechanical hyperalgesia and allodynia on the contralateral hind paw, further suggesting the contribution of central sensitisation. Our data provide strong evidence for a central contribution in both the rat UV-B pain model and an enhanced contribution in the new model combining UV-B irradiation with heat rekindling. We also elucidate potential differences in the methods used by ourselves and others to obtain mechanical withdrawal thresholds in rats, which may explain the lack of secondary hyperalgesia in the rat UV-B model.Copyright © 2011 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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