In this issue of the Scandinavian Journal of Pain, Rössler et al. describe an experimental model that confirms the central origin of pin prick hyperalgesia in the human sunburn model . UV-irradiation has been used extensively as a translational model for inflammatory pain and hyperalgesia using rodents [2,3], pigs  and human volunteers [5,6]. The time course of hyperalgesia development is similar in different species, with an onset latency of 3–6 h and a peak responsiveness 24–48 h after irradiation, thus representing a useful experimental model for drug testing. Upon irradiation of small skin patches (about 1cm2), only primary hyperalgesia has been detected in human and rodents [2,3]. As a multitude of mediators are being released upon UV-irradiation of the skin, including eicosanoids (e.g. PGE2, PGD2, PGF2a, LTB-4, 12-HETE), cytokines (e.g. IL-1, IL-6, IL-8, TNF-alpha), growth factors (e.g. TGF-beta, VEGF, NGF) vasoactive amines and neuropeptides (e.g.histamine, bradykinin, CGRP), researchers have mainly focused on the primary hyperalgesia that is evident in the inflamed skin. Some of these can be accounted for the in flammatory UV-induced responses, such as erythema (i.e. CGRP) or heat hyperalgesia (e.g. PGE2, bradykinin) and sensitization of heat-sensing ion channels (e.g. TRPV1). Another cardinal symptom of UV-inflammation
Scandinavian Journal of Pain – de Gruyter
Published: Jan 1, 2013
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