September 2009

Document Type


Degree Name



Dept. of Behavioral Neuroscience


Oregon Health & Science University


The disruption of memory retention following retrieval has been proposed to be due to the impairment of a memory reconsolidation process. Deficits in behavior attributed to reconsolidation have been demonstrated in a number of learning paradigms in animal models, including the associative learning that occurs between neutral stimuli and drugs of abuse. Because drug-associated stimuli can be a major factor in the persistence of addiction in humans, targeting potential reconsolidation mechanisms has been suggested as a potential target of pharmacotherapies aimed at dampening the powerful control of these stimuli over behavior. To that end, several studies have demonstrated impairment of reconsolidation as a means to reduce drug cue-mediated behaviors in animals using a variety of pharmacological treatments. The focus of this dissertation was to examine the role of the noradrenergic system as a potential mediator of the reconsolidation of drug memories using the conditioned place preference (CPP) paradigm using adrenergic receptor (AR) antagonists administered systemically and site-specifically into the basolateral amygdala, a brain region previously demonstrated to mediate reconsolidation. The non-specific β1/β2-AR antagonist, propranolol, when systemically administered following an initial test of cocaine CPP, attenuated preference during a subsequent test. This result was then replicated with systemic adminstration of the β2-AR antagonist ICI 118,551, but not the β1-AR antagonist betaxolol, demonstrating a β2-specific mechanism of the effect of propranolol. Furthermore, the α1-adrenergic antagonist prazosin, when administered post-test, also attenuated a subsequent preference.




School of Medicine



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