NEURAL & PAIN SCIENCES
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Man-Kyo Chung, PhD, DDS | Projects | Publications | Biography | Contact Information | | Neural & Pain Sciences |
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BIOGRAPHY
Our lab is interested in the function and modulation of nociceptive molecules in primary afferents. We study Transient Receptor Potential (TRP) channels in nociceptors primarily focused on TRPV1 and TRPA1. TRPV1 and TRPA1 are colocalized in a subset of sensory neurons having neurochemical properties of polymodal nociceptors. The pungency and pain induced by capsaicin is solely mediated by TRPV1 in mammal. TRPV1 can also be activated by noxious heat, and acid. Under inflammatory condition, signals from many inflammatory mediators converge to enhance the expression and function of this receptor resulting in the sensitization of nociceptors to thermal stimuli and thereby thermal hyperalgesia. Therefore, TRPV1 acts not only as a polymodal nocisensor but also the integrator of inflammatory signals. TRPA1 play critical roles as a sensor of tissue damage. TRPA1 is activated by remarkably various agents directly evoking pain and tissue damages such as natural pungent compounds (mustard oil, cinnamon, allicin, nicotine), an environmental pollutant (acrolein) and a toxic chemical (formalin). TRPA1 can also be activated by various endogenous substances that are generated under inflammation or injury such as H2O2, 4-hydroxynonenal, bradykinin, and prostaglandin J2. Also, a growing number of evidence shows the involvement of TRPA1 in mechanical and cold hyperalgesia under inflammatory or nerve injury conditions in experimental animals. Currently we study the function and modulation of TRPV1 and TRPA1 in the context of tooth pain. Also we are working on the electrophysiological characterization of desensitization properties of these channels.
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