Abstract
Burn injury induces pain and is frequently accompanied by persistent itch during wound healing. However, the underlying neural mechanisms remain poorly understood. Here, we developed a mouse model of post-burn pain and itch and examined changes in primary sensory neuron activity using in vivo calcium imaging of trigeminal ganglion (TG) neurons. To induce scald burn injury, anesthetized mice were exposed to boiling water on the cheek skin. Following injury, mice exhibited both spontaneous pain-related behaviors (wiping) and itch-related behaviors (scratching). Pain-related behaviors peaked on day 1 and returned to baseline within 5 days, whereas itch-related behaviors peaked on day 7 and persisted for up to 28 days. In vivo calcium imaging revealed a significant increase in the number of TG neurons exhibiting spontaneous activity on days 1 and 7 post-injury compared to baseline. While the proportion of capsaicin-sensitive neurons remained unchanged after scald burn, the proportion of chloroquine-sensitive neurons was reduced on day 1 and partially recovered on day 7. These findings suggest that enhanced spontaneous activity in primary sensory neurons may contribute to post-burn pain and itch. This model appears to be useful to investigate the neural mechanisms underlying sensory dysfunction following burn injury.