Instructor in Neurology
Dr. Wainger attended Princeton University and received an A.B. in Molecular Biology. He then earned M.D. and Ph.D. degrees at Columbia University where he worked with Dr. Steven Siegelbaum to study modulation of hyperpolarization-activated cyclic nucleotide-gated ion channels. He completed an internship in Medicine at New York Presbyterian Hospital, neurology residency in the Partners Neurology Program at Massachusetts General Hospital and Brigham and Women’s Hospital, and a fellowship in Pain Medicine at Massachusetts General Hospital. Dr. Wainger currently sees patients at the MGH Center for Pain Medicine in addition to working in the laboratory.
He is further developing the novel therapeutic approach of using the charged local anesthetic derivative QX-314 to pass through transient receptor potential V1 (TRPV1) channels, which are expressed exclusively in nociceptors, and thus produce pain-specific anesthesia. His project involves identifying additional intracellular-acting, membrane-impermeable agents that can be transmitted specifically into nociceptors through TRPV1 channels. He is also investigating potential new agonists for these channels. In a separate project, he is working to silence specific types of neurons in order to understand more clearly the contribution of these neurons to different sensory modalities. He uses electrophysiological, imaging, and behavioral approaches.
Santoro B, Wainger BJ, Siegelbaum SA. Regulation of HCN channel surface expression by a novel C-terminal protein-protein interaction. Journal of Neuroscience 24:10750-62, 2004.
Wainger BJ, DeGennaro M, Santoro B, Siegelbaum SA, Tibbs GR. Molecular mechanism of cAMP modulation of HCN pacemaker channels. Nature 411:805-10, 2001.
Notterman D, Young S, Wainger B, Levine AJ. Prevention of mammalian DNA reduplication, following the release from the mitotic spindle checkpoint, requires p53 protein, but not p53-mediated transcriptional activity. Oncogene 17:2743-51, 1998.