Effects of cocaine abstinence on BLA-mediated cocaine memory reconsolidation (2010)

Undergraduates: Kate Cowhey, Audrey Wells

Faculty Advisor: Rita Fuchs-Lokensgard
Department: Psychology & Neuroscience

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The reconsolidation hypothesis posits that after a memory is consolidated, it may become labile upon reactivation, and additional stabilization is required for the memory to be maintained. While a memory is in the reactivation-induced labile state, it is subject to disruption. Thus, maladaptive memories may be destroyed after original learning has occurred. Memory manipulation via pharmacological means is an exciting avenue of investigation for the treatment of many psychiatric disorders, including drug addiction. Cue-induced craving is a major contributing factor to drug-relapse, one of the biggest impediments of drug addiction treatment. Cocaine-associated contextual stimuli which serve as cues for drug-availability are sufficient to trigger relapse of drug-seeking behavior. However, drug-seeking behavior may be attenuated if context-drug association memories are disrupted after memory reactivation. Using an instrumental animal model of contextual drug relapse, we show that while the protein synthesis inhibitor anyisomycin infused into the basolateral amygdala (BLA) after reactivation of a cocaine-related memory effectively attenuates drug-seeking behavior after 1 day of forced abstinence, drug-seeking behavior is not diminished after 21 days of forced abstinence. These findings indicate that disruption of protein-synthesis dependent reconsolidation in the BLA does not produce long-term attenuation of context-induced drug-seeking behavior.