Dr. David W. Self, a NIDA-supported researcher, has received a Presidential EarlyCareer Award for Scientists and Engineers (PECASE) for his contributions to the field of drug abuse and addiction research. An assistant professor of psychiatry at the Yale University School of Medicine in New Haven, Connecticut, Dr. Self was one of 60 researchers who received awards from President Bill Clinton at a White House ceremony last December.
Dr. David Self receiving a Presidential Early Career Award for his contributions to drug abuse research. With him at the White House ceremony are Dr. Harold Varmus, director of the National Institutes of Health, left, and Dr. Jack Gibbons, science and technology advisor to the President.The annual Presidential Early Career Awards were established in 1996 to recognize and nurture individuals who have shown exceptional promise as leaders in scientific or engineering research. Candidates are nominated by Federal agencies, and awardees can receive up to $500,000 over a 5-year period to support their research.
The PECASE citation recognized Dr. Self's "outstanding basic research achievements that advanced our knowledge of the mechanisms underlying drug abuse and addiction through the innovative integration of state-of-the-art molecular biological techniques with sophisticated behavioral, pharmacological, and biochemical methods."
Dr. Thomas Aigner in NIDA's Behavioral Neurobiology Research Branch describes Dr. Self as an outstanding young neuroscientist who shows exceptional promise as a researcher. "He has already distinguished himself in many ways, even at this early stage of his career," says Dr. Aigner.
As a postdoctoral fellow in the Yale University laboratory of Dr. Eric Nestler, another NIDA-supported researcher, Dr. Self initiated a series of studies on drug relapse in animals. Previously, Dr. Self's innovative work earned him a NIDA First Independent Research Support and Transition (FIRST) Award. FIRST Awards support researchers who work independently of mentors and have no more than 5 years of research experience since completing their postdoctoral research training.
Dr. Self and his colleagues at Yale University's departments of psychiatry and pharmacology currently are conducting basic research that combines behavioral and biochemical studies to increase understanding of how drugs work to produce reward and addiction. With increased understanding of these basic mechanisms of addiction, new treatments can be developed.
"We are trying to identify the biochemical neuroadaptations, or changes in the brain's neurons, that result from chronic drug exposure, particularly exposure to cocaine," says Dr. Self. "We want to understand how these neuroadaptations affect the experience of drug reward, drug craving, or drug relapse associated with cocaine addiction."
"My role is to test how these neuroadaptations affect motivational states by integrating the molecular and biochemical information on cocaine's effects with an analysis of the drug's effect on behavior," he says.
Dr. Self and his colleagues reported preliminary results from this research last year in Science. They discovered that one particular dopamine receptor agonist, a compound similar to the brain chemical dopamine, could block cocaine-seeking behavior in rats while another enhanced cocaine seeking. These preliminary findings suggest that activating one particular dopamine receptor may prevent drug craving and ultimately prevent drug relapse, while activating another dopamine receptor may stimulate drug craving.
"We are exploring certain receptors that have not been examined before in humans in the hope of developing medications that can provide a new therapy for cocaine addiction," says Dr. Self.
Dr. Self earned a Ph.D. in pharmacology and toxicology at the University of California at Irvine. He received two NIDA Individual National Research Service Award Fellowships to support his predoctoral and postdoctoral studies.
Source
- Self, D.W.; Barnhart, W.J.; Lehman, D.A.; and Nestler, E.J. Opposite modulation of cocaine-seeking behavior by D1- and D2- like dopamine receptor agonists. Science 271:1586-1589, 1996.