Molecular mechanisms of cocaine memory reconsolidation (2012)

Undergraduates: Megan Blanton, Audrey Wells

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

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Cocaine addicts are particularly susceptible to cocaine-paired context induced relapse. This is due to the way cocaine associated memories are reconsolidated into long term memory storage following retrieval. The basolateral amygdala (BLA) is critical for reconsolidating cocaine memories that trigger instrumental cocaine seeking. The key to preventing cocaine-context induced relapse may be to inhibit this reconsolidation process. The molecule called extra-cellular signal related kinase (ERK) has been implicated in cocaine memory reconsolidation processes in the nucleus accumbens core (NACc), so we hypothesized that ERK may also be critical in reconsolidating cocaine-context memories in the BLA.
To test our theory, rats were trained to lever press for cocaine infusions in a distinct context, and then underwent extinction training in a novel context. After extinction training rats were exposed to the cocaine context, to destabilize cocaine-paired memories, or to a novel context so as to avoid memory reactivation. Directly after the reactivation session the rats were given micro infusions of an ERK inhibiter, U0126, or VEH into the BLA. Re-exposure to the cocaine-paired context induced robust cocaine seeking. Post-reactivation administration of U0126 decreased cocaine seeking behavior relative to VEH. This effect depended on memory reactivation because U0126 administration following novel context exposure did not alter further cocaine seeking behavior.