Dr. Richard Tsien
Dr. Richard Tsien is George D. Smith Professor of Molecular and Genetic Medicine in the Department of Molecular and Cellular Physiology at Stanford University. He was the initial Founder and Chairman of that Department and currently serves as Co-Director of the Neurosciences Institute at Stanford. A member of the U.S. National Academy of Sciences, Dr. Tsien is a world leader in the study of calcium channels and their signaling targets. He pioneered the area of channel modulation, demonstrating how neurotransmitters and drugs regulate Ca2+ channels through switching between gating modes. He deciphered how Ca2+ channels achieve exquisite selectivity yet high flux, demonstrating that carboxylate side chains of four glutamate residues form a unique pore locus for interaction with multiple permeant ions. By uncovering novel Ca2+ channels, he established the overall layout of the diverse Ca2+ channel family. Dr. Tsien discovered the branch exemplified by N-, P/Q- and R-type channels that is critical for fast neurosecretion. He elucidated distinctive features of each channel type, their functional importance and structure-function relations. He identified key downstream effector actions of Ca2+ entry, including calmodulin translocation to the nucleus as a key signal for control of gene expression. N-type channels are a target for pain therapy, while P/Q-type channels can be defective in migraine.
His current research focuses on fundamental mechanisms of neurotransmitter release and synaptic transmission at the level of single synapses. For example, Tsien’s group has described multiple modes of vesicle fusion, including a new mode known as “kiss-and-run.” Techniques and approaches include advanced electrophysiological and imaging techniques as well as molecular biology, immunocytochemistry and cDNA arrays. Possible modifications in neurotransmission in the setting of Down’s syndrome are a topic of considerable interest. Tsien is particularly interested in the possibility that abnormal synaptic signaling between neuronal cells may lead to cognitive dysfunction in Down syndrome.
