Characterisation of ultraviolet-B-induced inflammation as a model of hyperalgesia in the rat

T Bishop, DW Hewson, PK Yip, MS Fahey, D Dawbarn, AR Young, SB McMahon

Research output: Contribution to journalArticle (Academic Journal)peer-review

71 Citations (Scopus)

Abstract

In humans, the acute inflammatory reaction caused by ultraviolet (UV) radiation is well studied and the sensory changes that are found have been used as a model of cutaneous hyperalgesia. Similar paradigms are now emerging as rodent models of inflammatory pain. Using a narrowband UVB source, we irradiated the plantar surface of rat hind paws. This produced the classical feature of inflammation, erythema, and a significant dose-dependent reduction in both thermal and mechanical paw withdrawal thresholds. These sensory changes peaked 48 h after irradiation. At this time there is a graded facilitation of noxious heat evoked (but not basal) c-fos-like immunoreactivity in the L4/5 segments of the spinal cord. We also studied the effects of established analgesic compounds on the UVB-induced hyperalgesia. Systemic as well as topical application of ibuprofen significantly reduced both thermal and mechanical hyperalgesia. Systemic morphine produced a dose-dependent and naloxone sensitive reversal of sensory changes. Similarly, the peripherally restricted opioid loperamide also had a dose-dependent anti-hyperalgesic effect, again reversed by naloxone methiodide. Sequestration of NGF, starting at the time of UVB irradiation, significantly reduced sensory changes. We conclude that UVB inflammation produces a dose-dependent hyperalgesic state sensitive to established analgesics. This suggests that UVB inflammation in the rat may represent a useful translational tool in the study of pain and the testing of analgesic agents.
Translated title of the contributionCharacterisation of ultraviolet-B-induced inflammation as a model of hyperalgesia in the rat
Original languageEnglish
Pages (from-to)70 - 82
Number of pages13
JournalPAIN
Volume131 (1-2)
DOIs
Publication statusPublished - Sep 2007

Bibliographical note

Publisher: Elsevier

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