Johns Hopkins School of Medicine

Molecular and Cellular Mechanisms of Pain Sensation

My lab studies mechanisms underlying pain sensation.  One focus of the lab is a group of ion channel proteins of the Transient Receptor Potential Vanilloid (TRPV) family.  These channels share the intriguing feature that they can be activated by warm or painfully hot temperatures, as well as by many nonthermal stimuli. For example, TRPV1, the founding member of this family, can be activated by painful heat (>42°C), by protons, or by pungent chemicals such as capsaicin. This channel is strongly expressed in nociceptive neurons and is essential for normal behavioral responses to noxious heat. By examining these channels in recombinant and native systems, and taking advantage of knockout mice lacking one or more subtypes, we are dissecting the biological contributions of these channels to pain sensation and other processes in both neuronal and nonneuronal cells. A second focus of the lab is the use of cutting-edge molecular, cellular, genetic, behavioral and physiological approaches to understand the biological and pathophysiological basis of chronic pain in animal models and in human disease.

Current areas of emphasis include:

Understanding the mechanisms by which keratinocytes in the skin contribute to "indirect" pain perception by signaling to epidermal nerve endings under healthy conditions and in painful disease states in both animal models and human patients.
Uncovering non-nociceptive roles for TRPV channels in epithelial cells of the skin and urinary bladder.
Developing novel assays and reagents for the quantification and characterization of acute nociception and chronic pain
Dissecting the cellular and molecular events that contribute to neuropathic pain and exploring strategies to reverse this condition