LB1006 Mouse model of post-burn itch

Abstract

The majority of the post-burn patients suffer from chronic itch, which is often resistant to antihistamine treatment. Post-burn itch involves sensitization of itch-signaling pathways, leading to ongoing itch and alloknesis (touch-evoked itch), but the underlying mechanisms behind post-burn itch are largely unknown. We have developed a novel animal model to investigate the neuronal mechanisms of post-burn itch. A scald burn injury was produced in adult C57BL/6 mice by exposing the shaved back skin to boiling water. The burn surface area was over 150 mm2 on Day 1, decreased to 30 mm2 on Day 14, and then remained at a plateau. To assess spontaneous scratching, mice were videotaped on Days 0, 1, 3, 5, 7, 10, 14, 21, and 28 after the scald burn treatment. Counts of spontaneous scratch bouts increased transiently on Days 1, 3, and Day 5 compared to Day 0, returned to the basal level by Day 10, and reincreased significantly on Days 14, 21, and 28. To test for alloknesis, a weak von Frey filament (VF; 0.7 mN) was repeatedly applied to post-burn skin on Days 0, 1, 3, 5, 7, 14, 21, and 28 after the scald burn treatment, and the presence or absence of evoked hindlimb scratch bouts was noted (VF stimulation does not elicit any response in naïve C57BL/6 mice). VF-evoked scratching increased significantly on Days 21 and 28. The histamine H1 receptor antagonist chlorpheniramine was tested on Day 22 but did not inhibit spontaneous scratching, suggesting that non-histaminergic itch pathways are involved in post-burn itch. This new animal model appears to be useful for investigations of post-burn itch and sensitization of itch-signaling pathways.