This review reveals that there are presently key limitations to our understanding of glutamate’s role in the development of alcohol dependence and the impact that genetics has on this process. First, there are no studies examining glutamate-associated gene and/or protein expression changes across the juvenile, adolescent, emerging adult, and full adult stages of development. This information is crucial given the fact that the risky drinking age-of-onset is inversely associated with the probability of developing alcohol dependence (i.e., earlier onset leads to higher risk of developing alcoholism). And, while there is some evidence for an association between being a FHP individual and initiating risky drinking at a younger age, findings comparing the effects of ethanol on glutamate function between FHP individuals/models and FHN individuals/models are very limited. Second, studies thus far have been limited to gross examinations of regions and/or subregions of major structures in the central reward neu-rocircuitry. Also related to this point, a third limitation is the lack of publications examining multiple regions (i.e., putative circuits) within a single study. Despite these limitations, substantial progress has been made with
