Neuroimmune interactions are of known importance in the genesis and maintenance of inflammatory pain states. However, the immune response to tissue damage is likely to differ depending on whether or not the injury is accompanied by infection. Many clinically important inflammatory pain states involve a sterile tissue injury. However, existing animal models of cutaneous inflammatory pain use injuries that are likely to involve those components of the immune system that are specialized for combating pathogens (e.g., injections of Complete Freund's Adjuvant, carrageenan, or zymosan). We describe here a model of cutaneous inflammatory pain in the rat produced by a sterile injury evoked by a single exposure to ultraviolet irradiation. The animals develop heat-hyperalgesia, mechano-hyperalgesia, mechano-allodynia, and cold-allodynia that last for several days. Cold-allodynia appears within 6 h or less, but the other symptoms are not clearly evident until 12-36 h after exposure. This model offers several advantages for the experimental analysis of the causes of inflammatory allodynia and hyperalgesia.