Thus, findings derived largely from basic science studies have indicated that alcohol is experienced differently by adolescents and adults, and similar hints can be found in the limited human research literature as well. Adolescents are primed to be particularly sensitive to alcohol’s social-facilitatory and (possibly) rewarding effects, while being more resistant than adults to its aversive, sedating, motor-impairing, and socially suppressive consequences. As mentioned earlier, these differential ontogenetic sensitivities may be related in part to the developmentally enhanced portions of the glutamate excitatory system and developmentally immature components of GABA inhibitory systems that are characteristic of the adolescent brain. Developmental alterations in other neurotransmitter systems upon which alcohol exerts its effects (e.g., opiate, cannabinoid, and DA systems) may also contribute to adolescent-related alcohol sensitivities. There is evidence, for example that certain components of the opiate system contribute to alcohol-related social facilitation seen in rats during adolescence (Varlinskaya & Spear, 2010). It is also possible that some adolescent-typical sensitivities to alcohol may reflect broad developmental alterations in DA projection systems and their neural targets in the nucleus accumbens, PFC, and amygdala
