Lesion studies in laboratory animals have revealed that motivationally oriented behaviors towards natural rewards and drugs can be partitioned into a diversity of psychological components, each with complex, sometimes overlapping, and incompletely understood neural representations (e.g., Baxter & Murray, 2002; Cardinal et al., 2002). There is continuing controversy, however, as to the nuances of how reward-related processes should be parsed, the roles of specific neural components in these separable processes, and the identification of the constituents that become dysfunctional during the development of addiction (e.g., see Berridge, 2007). For instance, one influential theory views DA projections to forebrain as critical for mediating the hedonic impact of rewards, with repeated drug use inducing a hypo-DA state, leading to a decrease in sensitivity to natural and drug rewards that in turn promotes elevations in drug use to counter this insufficiency (e.g., Volkow et al., 2007). This hypothesis is wildly different from another prominent perspective that views these DA projections as critical for the attribution of incentive salience, and hence motivational drive, to reward-related stimuli; this theory posits that repeated drug use increases
