I conduct translational research that rests at the intersection of psychology, pharmacology, and genetics. My work is focused on understanding the neural mechanisms responsible for decision-making and impulsivity in relation to drug and alcohol abuse and on developing novel treatment strategies for these disorders. Our group uses a combination of behavioral pharmacology, genetics, electrophysiology, and fMRI to conduct research in both animal and human models of choice. By integrating the pharmacological and genetic results of animal studies with human traits such as impulsivity, time perspective, and delay-discounting, it becomes possible to determine potential mechanisms by which motivation and preference can be altered.
For example, we have recently shown that there is robust individual variability in an animal model of preference and aversion following the administration of the non-specific opioid antagonist naltrexone. Our evidence suggests that this variability may result from differences in the distribution and/or the function of mu-opioid receptors within key regions of the CNS reward pathway. We have obtained similar results in a human model of alcohol self-administration and have successfully correlated naltrexone-induced aversion with baseline ethanol consumption in both species. We have also been able to show that the endogenous opioid system contributes to the performance of a delay-discounting task in humans and that this performance can be altered by a single administration of naltrexone. We are now looking at differences in the BOLD signal in human alcoholics following naltrexone administration and comparing this to the activity we see in healthy controls. Together, these results indicate a mechanism by which endogenous opioids affect decision-making and preference and may point the way toward the development of novel therapeutic targets for drug and alcohol addiction.