Humans rely on the sensations of itch, touch and pain for a broad range of essential behaviors. For example, acute pain acts as a warning signal that alerts us to noxious mechanical, chemical and thermal stimuli, which are potentially tissue damaging. Likewise, itch sensations trigger reflexes that may protect us from disease-carrying insects. In addition, during inflammation or injury, we experience a heightened sensitivity to touch that encourages us to protect the injured site. Despite these essential protective functions, itch and pain can outlast their usefulness and become chronic. In mammals, these sensations are mediated by specialized subsets of somatosensory neurons that innervate the skin and viscera. Non-excitable cells, such as keratinocytes and immune cells, also work in conjunction with somatosensory neurons to promote acute and chronic inflammatory pain and itch.
My lab aims to identify the mechanisms by which neurons, immune cells and epithelial cells detect itch, pain and tactile stimuli, under normal and pathophysiological conditions. We use a combination of cellular physiology, molecular biology, molecular genetics and behavioral studies to probe the cellular and molecular mechanisms that mediate itch, touch and pain.
In the News
Some 10 percent of the population suffers from eczema at some point in their lives. The chronic skin condition, for which there are no cures or good treatments, causes symptoms ranging from dry, flaky and itchy skin to flaming red rashes and, particularly in children, nasal allergies and asthma.
A new study of itch adds to growing evidence that the chemical signals that make us want to scratch are the same signals that make us wince in pain.
Three UC Berkeley faculty members - Diana Bautista, Amy Herr and Donald Rio - have been singled out as innovators by the National Institutes of Health and will receive special grants designed to fund "transformative research" that could lead to major advances in medical science.