Abstract
Theories of drug addiction that incorporate various concepts from the fields of learning and memory have led to the idea that classical and operant conditioning principles underlie the compulsiveness of addictive behaviors. Relapse often results from exposure to drug-associated cues, and the ability to extinguish these conditioned behaviors through inhibitory learning could serve as a potential therapeutic approach for those who suffer from addiction. This review will examine the evidence that extinction learning alters neuronal plasticity in specific brain regions and pathways. In particular, subregions of the prefrontal cortex (PFC) and their projections to other brain regions have been shown to differentially modulate drug-seeking and extinction behavior. Additionally, there is a growing body of research demonstrating that manipulation of neuronal plasticity can alter extinction learning. Therefore, the ability to alter plasticity within areas of the PFC through pharmacological manipulation could facilitate the acquisition of extinction and provide a novel intervention to aid in the extinction of drug-related memories.
Highlights
Theories of drug addiction that incorporate various concepts from the fields of learning and memory have led to the idea that classical and operant conditioning principles underlie the compulsiveness of addictive behaviors
In this review, we focused on studies that incorporate learning principles in extinction training with the goal of lessening the influence of these cues on addictive behavior
It has been widely recognized that drug use and relapse are strongly cue specific (Drummond and Glautier, 1994) and one of the most important factors that contributes to relapse is the impact of drug cues on drug-seeking behavior
Summary
Extinction learning and the prefrontal cortex in addiction this review is on the extinction of drug-seeking behavior, observations from the fear/non-drug extinction field will be incorporated where appropriate. Infusion of the beta-receptor agonist clenbuterol into the IfL cortex facilitates extinction of cocaine-seeking behavior (LaLumiere et al, 2010) These studies add support to the growing body of evidence that areas of the PFC are heavily involved in extinction behavior, and one possible mechanism could be noradrenergic-related changes in this region. Systemic administration of the HDAC3 inhibitor RGFP966 facilitates the extinction of a cocaine-related memory, and it was suggested that this effect was mediated by enhancement of memory consolidation during extinction learning (Malvaez et al, 2013) These effects were associated with histone acetylation linked to gene expression in the IfL cortex, hippocampus, and NAc. Taken together, observations from the fear and addiction fields have provided intriguing insights into the possible therapeutic targets related to epigenetics that could potentially be utilized to facilitate the extinction of emotionally salient memories. While there is excitement in the field that revolves around the influence of reconsolidation on extinction behavior, more research is clearly needed to fully elucidate the contributions of both processes in the inhibition of behavior
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