Reinforcement-mediated associative learning, or the ability to ascribe deterministic relationships between environmental stimuli that signal the probability of receiving a primary reinforcer (e.g. food), has been divided into 3 components or stages [1]. The first, unlearned stage is the organism's experience with a primary reinforcer that elicits some unlearned/innate physiological response (e.g. palatability of a food or satiety). The second phase involves the attachment of salience to external stimuli (discriminative stimuli) that signal whether the delivery of a primary reinforcer will or will not occur based on some emitted behavior (e.g. a rodent lever presses for food pellets only when a stimulus light is illuminated in an operant chamber). Finally, there is the maintenance of associative learning relationships over time (a stimulus light always signifies a food pellet is available subsequent to a lever press) [see refs. [1,2] for review]. Berridge and Robinson [1] have proposed that dopamine plays a pivotal role in the second phase of reinforcement-mediated associative learning by molding the "incentive salience" or learned motivational properties of conditioned stimuli. In support of this view are several studies demonstrating that the disruption of dopamine signaling via acute blockade of dopamine receptors with dopamine receptor antagonists [3-9] or 6-OHDA lesions [1,10,11] do not disrupt phase 1, the palatability or primary reinforcing characteristics of a natural reinforcer (e.g. palatability) but disrupt phase 2, the formation of incentive salience.