Research Description

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. This development of a strong drug cue preference is a potent learning mechanism which accelerates the transition from voluntary drug use to drug addiction. Addiction can be conceptualized as a progressive phenomenon initiated and maintained by the conditioned rewarding effects of drugs of abuse. Drug conditioning induces changes in synaptic plasticity which endure even after long periods of drug abstinence. As a result of this plasticity in motivational and cognitive circuits, exposure to drug cues previously can evoke drug craving and seeking responses and that can reinstate drug taking.

Extinction is behavioral approach to reduce or eliminate conditioned preferences to drug associated environment. It is defined as a new learning process that results in a decrease in frequency or intensity of previously learned responses. Extinction occurs after repeated drug cue exposure without the drug that originally reinforced approach/preference learning. We hypothesize a role for gamma-aminobutyric acid- (GABA) type B and N-methyl-D-aspartate receptor neurotransmission in the development and extinction of conditioned opiate reward. We examine the effects of GABA and NMDA receptor agents on the acquisition and expression of opiate and cocaine reward and self-administration, their extinction, and and reacquisition. We are interested in understanding how these agents alter addiction-related learning processes and neural plasticity in circuits mediating motivational and cognitive functions. 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.