My lab investigates the molecular basis of neuronal electric excitability. We explore the molecular mechanism with which cells detect environmental stress. Our primary research focus is sensory transduction, the process by which primary sensory neurons generate electric signals. We use a variety of methods ranging from molecular biology, physiology, pharmacology to biophysics to dissect the transduction mechanism.
Sensory transduction typically starts from activation of modality-specific receptors in specialized nerve fibers. Many receptors involved in transduction processes are transient receptor potential (TRP) family ion channels. At the protein level, these sensory transducers contain individual structural modules of distinct functions. Biochemical modification of transduction channels further broadens their sensitivity and response intensity, which accounts for alteration of our subjective perception of the external world during physiological adaptation of healthy individuals or progression of disease. Expectedly, they are fundamental principles which new treatments of sensory dysfunction must base on. We hope to apply the knowledge from our laboratory work to the development of new molecules useful for treatment of chronic pain by selective silencing of aberrantly hyperactive nociceptors.
Quantitative analysis of receptor-effector coupling: The nervous system contains only a limited number of transmitters and ion channels. How can receptor-effector communication exhibit remarkable plasticity with rich complexity and broad dynamic ranges but still manage to maintain the robustness? We take two complementary approaches, combinatorial expression and biochemical reconstitution, to address this question. Receptor-effector complexes are artificially assembled through heterologous expression in either whole cell-based or cell free biochemical systems to determine the contribution of molecular compositions of signaling complexes to coupling efficiency between receptors and effectors.