How developmental alterations in these DA projections to reward-relevant forebrain regions might influence reward-related behavior during adolescence is unclear. Should these changes reflect a hyposensitivity of DA systems, a disruption in the attribution of incentive salience or expression of goal-directed behavior during adolescence might result (e.g., see Berridge, 2007). Alternatively, any adolescent-associated DA hyposensitivity could be hypothesized to lead to an attenuated sensitivity to natural or drug rewards, intensifying drug use to compensate for this reward deficiency (akin to theories of addiction as representing reward deficiencies --e.g., Volkow et al., 2007). Yet, there are many other potential “players” in reward-associated regions that also change during adolescence. Consider, for example, the cannabinoid system, with receptors (CB1-Rs) that are largely localized to presynaptic endings where they serve as important regulators of neural inputs to DA target regions (Cohen et al., 2008). CB1-Rs peak developmentally in striatum and limbic regions during adolescence (P30–40 in rats), before declining significantly to reach adult levels (Rodriguez de Fonseca et al., 1993). Notable developmental transformations in endocannabinoid levels also are evident during adolescence, with, for instance, developmental
