Human genetics is uniquely suited for associating disease states with specific genes and polymorphisms. Model organisms can identify genes that can alter disease-related phenotypes. Model organisms can also be used to test whether the polymorphisms found in humans are plausible causes of the human phenotypes and can provide mechanistic insights that would be hard to obtain using humans. For psychiatric traits such as substance abuse, it is difficult to relate the human and mouse phenotypes, for this reason it is important to understand the relationship between mouse behavioral paradigms and the various component processes that contribute to substance abuse. Intermediate phenotypes in humans such as those outlined in Table 1 can be helpful for connecting disease diagnoses to animal behavioral paradigms. In this review, we have focused on single genes as the unit of analysis and translation. This decision was partially dictated by the published literature that we are reviewing. It is easy to imagine that biological pathways could also be used such that interacting neigh bors of an implicated gene might also be investigated in the complimentary species; as
