We investigated the role of the C-fiber barrage in the development of hyperalgesia in rat tails exposed to ultraviolet A (UVA)-light exposure by pre-emptively blocking C-fiber activation with the local anesthetic bupivacaine. Thirty minutes before UVA-light exposure, male Sprague-Dawley rats were given subcutaneous injections, in the base of the tail, of either saline or bupivacaine (1 mL of .5%). Thermal hyperalgesia was assessed daily from day 1 to day 10 after UVA-light exposure by measuring response latency to noxious heat (tail immersion in 49 degrees C water). Injection of bupivacaine completely prevented the development of thermal hyperalgesia (P < .05, main effect of group, 2-way analysis of variance). Primary mechanical hyperalgesia was assessed daily from day 1 to day 14 after UVA-light exposure by measuring aversive behavior responses to a punctate pressure applied to the tail with a von Frey anesthesiometer. The rats given bupivacaine developed hyperalgesia to the mechanical challenge that persisted for 14 days (P < .05, main effect of time, 2-way analysis of variance) and was identical to the hyperalgesia developed by the rats given saline. We concluded that the C-fiber barrage is involved in the development of thermal hyperalgesia but not sustained primary mechanical hyperalgesia, induced by exposing rats' tails to UVA light.
Perspective: UVA-light exposure of the rat tail causes prolonged hyperalgesia to noxious thermal and mechanical challenges. We have demonstrated that the C-fiber barrage is involved in the development of sustained thermal hyperalgesia, but not mechanical hyperalgesia, caused by exposure of the rat tail to UVA light.