BACKGROUND: Previous reports have described that the local administration of opioid receptor agonist can attenuate the nociceptive responses induced by a variety of inflammatory states. This study evaluated the effects of mu or kappa opioid receptor agonists peripherally administered at a site of injury on the state of thermal hyperalgesia induced by mild burn injury. METHODS: Thermal injury was induced after briefly anesthetizing with halothane, by applying the left hindpaw to a hot plate (52.5 degree C) for 45 seconds. Paw withdrawal latency of the hindpaw was determined using an underglass thermal stimulus, which allowed the response latency of the injured paw to be obtained. In this work, the mu receptor agonist, morphine (10, 30, 100 microgram), or the kappa receptor agonist, U50,488H (10, 30, 100 microgram), was administered respectively at the injured site on the right hindpaw in rats. To compare the systemic effects of the drug, the same drug was administered at the normal left hindpaw site with mild burn injury. Naloxone (40 microgram/kg) was administered at the injured site or at the normal site to determine the reversibility of the opioid used. RESULTS: Mild burn injury produced thermal hyperalgesia manifested as reduced paw withdrawal latency. Administration of either morphine (10, 30, 100 microgram) or U50,488H (10, 30, 100 microgram) at the injured site attenuated hyperalgesia in a dose-dependent manner. But the administration of drugs at the normal site had no effect on hyperalgesia at the injured site. In addition, naloxone had the effect of morphine and U50,488H reversed significantly. CONCLUSIONS: These results suggest that peripheral mu or kappa opioid receptor administration at an injured site may play an important role in the hyperalgesia induced by mild burn injury.