Itch is an unpleasant somatic sensation that causes a desire to scratch, and it is speculated to serve as a self-defense system to remove harmful substances from the skin and mucous membranes. However, chronic itch associated with allergic dermatitis, including atopic dermatitis, causes extremely intense and prolonged itch and scratching, which significantly reduces the patient’s quality of life. Therefore, chronic itch needs to be properly removed, but in many cases they do not respond to antihistamines, the typical itch medications, and there are few effective treatment options.
Recent studies have identified the gastrin-releasing peptide receptor (GRPR) expressed on spinal dorsal horn neurons as an itch-specific receptor. However, among the many pruritogens and chronic itch models, Grpr deficiency suppressed only itch behaviors induced by a small number of pruritogens and chronic itch models, and these suppressions were partial. Thus, we have attempted to identify a subset of spinal dorsal horn neurons that contribute to GRPR-independent itch. In this talk, we will detail our newly identified subset of spinal dorsal horn neurons that contribute to GRPR-independent itch.