Involvement of Nuclear Factor-κB in Cocaine Memory Reconsolidation (2013)

Undergraduates: Victoria Greene, Audrey Wells

Faculty Advisor: Rita Fuchs Lokensgard
Department: Psychology & Neuroscience

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Associations between contextual drug-paired cues and reinforcing drug properties are stored in long-term memory and strengthened by memory reconsolidation. During this process, memories are re-stored after retrieval. In disruption of this process, removing anticipatory factors of contextual cues is possible. Previous research has shown the basolatateral amygdala (BLA) is central for memory reconsolidation. It is the goal to pinpoint the intracellular processes causing reconsolidation of drug memories that promote relapse in the BLA. We hypothesized that the Nuclear Factor-κB (NF-κB) is required for reconsolidation of cocaine memories, and when inhibited following reactivation, context-induced cocaine-seeking behavior would reduce. Rats were trained to self-administer cocaine in a one context and then underwent extinction training, rehab, in a different context and then were briefly re-exposed to the drug-paired context (i.e., reactivation) and infused with either NF-κB inhibitor (sulfasalazine; 0.2 or 2 µg/0.5 µl/side) or 20% DMSO vehicle (VEH) into the BLA. A test of cocaine-seeking behavior in the cocaine-paired context was administered ~72 h later. During this test, previously VEH-treated rats exhibited cocaine seeking, but neither dose of sulfasalazine significantly altered responding relative to VEH. These results are useful in furthering the knowledge of how reconsolidation works on a cellular level, as future research continues to pinpoint the mechanisms involved.