Research & Publications
In my laboratory we are interested in how humans and animals sense touch and pain. These fundamental sensations originate in peripheral sensory neurons which contain signaling pathways that translate environmental stimuli into neural activity. Our aims are to identify the molecular components of these pathways and to understand how sensory neurons become sensitized during injury and chronic painful conditions such as inflammation. In our current studies we use pharmacological, molecular genetic and physiological approaches as well as fluorescent imaging techniques to investigate the properties of ion channel proteins that serve as sensors for temperature and noxious stimuli in sensory neurons. These proteins belong to the gene family of TRP (transient receptor potential) ion channels, some of which are the targets of natural plant products that activate the sensation of heat and pain (capsaicin, mustard oil) or cold (menthol). We are using these compounds as chemical probes to study how TRP channels are activated, how they interact with endogenous ligands and how temperature sensing occurs. Another goal in our lab is to understand how signaling pathways are used to increase TRP channel activity in disease. TRP channels are regulated by other receptor systems through membrane phospholipid turnover, kinase pathways and endogenous ligands. Increased channel activity results in neural sensitization that causes hypersensitivity to sensory input and contributes to painful inflammation by a mechanism known as neurogenic inflammation. This mechanism is important for conditions such as arthritis, vasculitis, psoriasis, intra- and postoperative pain, trauma, invading cancer and visceral and musculoskeletal disorders. With our studies we hope to gain new mechanistic insights into neurogenic inflammation, identify potential pharmacological targets and reveal basic molecular and cellular mechanisms of sensory transduction.