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Abstract

Disrupting memory after retrieval is thought to reflect impairment of reconsolidation, a process that restabilizes memories and can sustain drug cue–controlled behavior. Because drug‑associated stimuli contribute to persistent addiction, pharmacologically targeting reconsolidation is a promising therapeutic strategy. This dissertation investigates the role of the noradrenergic system in reconsolidation of drug memories using the conditioned place preference (CPP) paradigm. Adrenergic receptor antagonists were administered systemically and directly into the basolateral amygdala, a key reconsolidation locus. We evaluated whether blocking noradrenergic signaling at retrieval attenuates subsequent CPP expression, thereby weakening drug cue–memory strength. Findings aim to clarify noradrenergic mechanisms that support reconsolidation and to identify adrenergic targets with potential for pharmacotherapies that reduce the motivational impact of drug‑paired cues.

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