Alcohol overconsumption is a widespread problem, and understanding both the underlying causes of this maladaptive behavior and the adverse impacts on the brain after alcohol use is therefore important to reducing societal costs. This dissertation reviews the evidence for a link between an early environmental disruption, prenatal stress (PNS), and changes in behavior towards drugs of abuse, including alcohol. Further, it reviews a facet of the PNS phenotype, reductions in the adult neural stem cell (NSC) population, which might contribute to this change, as well as the current evidence for the impact of alcohol on the adult neurogenic system. Given that NSCs are a converging biological target of both PNS and alcohol, it is hypothesized that these cells are a critical mediator of PNS-enhanced alcohol-seeking. Presented here are empirical studies which clarify the functional links between alcohol, prenatal stress, and the adult neurogenic system. The broad aims were to determine whether: 1) Alcohol impacts NSCs in the adult neurogenic system, 2) PNS increases alcohol consumption and seeking, 3) PNS decreases proliferation of NSCs in the adult neurogenic system, and 4) Ablation of the adult neurogenic system mimics the impact of PNS on alcohol seeking and consumption. These studies found that alcohol itself does reduce NSC proliferation and PNS does increase alcohol-seeking behaviors and reduce NSC proliferation, but that ablation of adult NSCs does not reproduce the increased alcohol-seeking component of the PNS phenotype. The results are discussed in terms of their implications for the overarching hypothesis of this dissertation, including a re-evaluation of the linkage between PNS-induced changes in NSCs and alcohol seeking, other mechanisms by which PNS might be changing the alcohol-seeking phenotype, and further implications for the study of alcohol's effects on neural systems.