ABSTRACT Cue-reward associations are critical for developing adaptive responses to cues that signal the availability of food, mating opportunities, and other rewards. During associative learning, cues acquire predictive value, meaning they become linked to an explicit representation of the outcome, but in some instances, they may also acquire incentive salience, meaning they take on some of the attractive and motivational properties of the reward. The excessive attribution of incentive or motivational value can result in cues gaining excessive control over behavior, and lead to maladaptive responses such as those associated with addiction. But the propensity to attribute cues with incentive salience is highly variable and seems to greatly depend on the way individuals learn cue-reward associations. Using the “sign- and goal-tracking” rat model of associative learning we can specifically study individual variation in the propensity to attribute incentive salience to reward cues, and dissect the neurobiological mechanism underlying predisposition to cue-driven psychopathologies like addiction. Compared to “goal-trackers” (GTs), “sign-trackers” (STs) not only use reward cues as predictors, but also attribute them with incentive salience and find them rewarding, resulting in increased motivation towards and fixation on these cues. STs are more impulsive as well as susceptible to cue-induced reinstatement or “relapse” of drugs of abuse when compared to GTs, making this an excellent model to study predisposition to addiction-like behaviors. The focus of this proposal is on the nucleus accumbens (NAc), a region known to be a critical component of the “motive circuit”. STs and GTs exhibit different cue- and reward-evoked patterns of activity in the NAc during Pavlovian learning, but it remains to be determined what neurobiological mechanisms give rise to these different NAc activity profiles and how they may account for the ST/GT phenotype. The proposed experiments will test the hypothesis that there are functional differences between STs and GTs in the strength of synaptic inputs to the NAc, particularly from regions like the ventral hippocampus (vHPC), which is known to be necessary for the attribution of incentive salience. Determining the specific neuronal properties and neural pathways involved in the attribution of incentive salience will increase our understanding on the specific risk factors associated with addiction vulnerability and lead to better biomarkers and tailored therapeutic approaches to treat individuals at higher risk of addiction.