Cell Biology, Neurobiology & Anatomy

Cheryl L. Stucky, PhD Professor Director, Neuroscience Doctoral Program Neuroscience Doctoral Program website Department of Cell Biology, Neurobiology & Anatomy Medical College of Wisconsin 8701 Watertown Plank Road Milwaukee, WI 53226-0509 Phone: (414) 955-8373 FAX: (414) 955-6517 email: cstucky@mcw.edu List of publications Recent interviews: International Innovation 2011

Education:
PhD, University of Minnesota, Minneapolis, 1995
Postdoctoral, University of Würzburg, Würzburg, Germany and Max Delbrück Center for Molecular Medicine, Berlin, Germany

Graduate Programs:
Director of Neuroscience Doctoral Program
Program in Cell and Developmental Biology

Research Area: Molecules that sense touch and pain

Positions are currently available for PhD students 

Please contact Dr. Cheryl Stucky at cstucky@mcw.edu

In virtually all of our daily activities, we rely on our skin and nervous system to interact with the world around us. Our laboratory is keenly interested in how our skin sensory neurons detect environmental stimuli, such as tactile pressure, cold and heat, and painful stimuli. The best candidate proteins for transduction of physical stimuli are members of the Transient Receptor Potential ion channel family. For example, we recently showed that the Transient Receptor Potential Melastatin 8 (TRPM8), the receptor activated by menthol and peppermint, is a key receptor that detects cool and painfully cold stimuli (Bautista et al., 2007, Nature).

A major current challenge in sensory neurobiology is to identify the molecules that allow us to sense mechanical stimuli (from light touch to painful pressure). Our laboratory recently determined that the Transient Receptor Potential Ankyrin 1 (TRPA1) receptor is required for pain-sensing neurons in the skin to detect painful pressure. We use a unique “skin-nerve” experimental technique, whereby we can record and quantify the responses of single skin sensory neurons to natural stimuli like mechanical pressure. We combined this technique with a transgenic mouse that lacks the TRPA1 channel to demonstrate that TRPA1 is critically required for pain receptors to respond to force (Kwan et al., 2009, Journal of Neuroscience). In parallel, we showed that a chemical blocker of the TRPA1 channel inhibits mechanical responses in pain-sensing neurons from wild type mice (Kerstein et al., 2009, Molecular Pain). On a cellular level, we use patch clamp recordings of single neurons to determine the contribution of TRPA1 to mechanical currents in the plasma membrane (Vilceanu and Stucky, PLoS ONE, in press).

We are now using these techniques, transgenic mice and pharmacological blockers in translational studies to determine whether the TRPA1 channel is responsible for touch-evoked pain in several mouse models of chronic pain. These models include mice with severe sickle cell disease, neuropathic (nerve injury) pain, and cancer tumor pain. Over 50% of people suffer from chronic pain at some point in life, and chronic pain is the most common reason people go to a doctor for a problem. Our hope is that our studies will provide evidence for the clinical utility of TRPA1 blockers in human patients with chronic touch-induced pain.