When individuals come into contact with environmental cues or contexts where drugs of abuse are administered, future exposure to these same cues elicit conditioned approach behaviors via associative learning processes. Addiction can be conceptualized as a progressive phenomenon initiated and maintained by the conditioned rewarding effects of drugs of abuse. As a result of neural plasticity in motivational and cognitive circuits, exposure to drug cues previously can evoke drug craving and seeking responses and that can reinstate drug taking. Our research examines the effects of gamma-aminobutyric acid- (GABA) type B and N-methyl-D-aspartate receptor receptor agents on the acquisition and expression of opiate and cocaine reward, self-administration, their extinction, and reacquisition. Such research defines the mechanisms related to drug relapse and defines novel therapeutic targets of interest for clinical studies. We utilize state-of-the-art methods in behavioral neuroscience, neuroanatomy, and neurochemistry to study these signaling pathways and circuitry in addiction.

Our clinical lab is involved in translational research that examines tobacco cue reactivity in schizophrenic smokers along with alterations in reward involved with other environmental cues in this population. Our translational work uses "bench to bedside" approaches in examining the neurobiological mechanisms of addiction and related behavioral and neuropharmacological treatment approaches to this chronic relapsing disorder of addiction.