RELATED STORY: Jon Levine: A Passion for Deciphering Pain
Jon Levine received a B.S. in biophysics and an M.S. in bioengineering from the University of Michigan, and earned a Ph.D. in neurobiology at Yale University, where he worked with Robert Wyman. He conducted postdoctoral research on Drosophila neurogenetics in Donald Kennedy’s laboratory at Stanford University. Levine completed his medical training at the University of California, San Francisco, where he was also a fellow in rheumatology and clinical pharmacology. He joined the faculty of UCSF in 1983. In addition to a Rita Allen Foundation award, Levine has received a Chancellor’s Commendation for Research Excellence from the University of California, a Hartford Foundation fellowship, and a Frederick W.L. Kerr Basic Science Research Award from the American Pain Society.
Levine’s laboratory employs a multidisciplinary approach of molecular, biochemical, in vitro and in vivo electrophysiological and behavioral techniques to evaluate mechanisms underlying pain and analgesia. His team is investigating signal transduction mechanisms for mechanical, thermal and chemical stimulus-induced activation of sensory neurons and mechanisms underlying sensitization of responses to these stimuli. They have described a novel transducer mechanism for mechanical stimuli, as well as second messenger pathways mediating nociceptor sensitization in inflammatory and neuropathic pain. They are investigating the modulation of transduction by opioids, including the mechanisms underlying opioid tolerance and dependence. Levine’s group also studies central nervous system circuits that mediate analgesia, and has described a novel analgesia circuit involving limbic pathways, as well as sexual dimorphism in pain and analgesic mechanisms. Finally, they are investigating neural and endocrine (stress axis) contributions to inflammation and the immune response. Their work has elucidated a physiological mechanism consisting of a negative feedback inhibition of the inflammatory response, involving neural and endocrine mechanisms.