The past decade has evidenced a great deal of research related to the effect of prenatal alcohol exposure on fetal growth and development in animals. As a result, it is clear that ethanol is a teratogen in the classical sense of producing birth defects. Also, some types of behaviors are abnormal and an elevated stress response follows some types of stressors. Data regarding whether prenatal alcohol exposure alters the offspring's response to subsequent alcohol challenge are inconsistent. The present proposal attempts to develop a more complete picture of the teratogenic effects of ethanol by utilizing a mouse model to address the above three issues, namely behavioral impairment, alcohol sensitivity, and stress responsiveness. Moreover, a single appetitively-motivated conflict task that does not employ shock will be used. The behavioral paradigm is referred to as negative contrast. This task permits quantification of how animals respond to an abrupt reduction in expected reward. Specifically, the consummatory performance of animals that are downshifted from a preferred to a less preferred reward is greatly depressed in comparison to animals that are not shifted, but receive experience with only the less preferred or smaller reward. That is, while the smaller reward is relatively not as rewarding as that previously experienced by shifted animals, it does, itself, have some intrinsic rewarding property since unshifted animals will readily consume it. Thus, the task engenders a consummatory conflict situation (as evidenced by elevated plasma corticosterone levels), since both rewards may be considered to be "rewarding." In fact, ethanol has been shown to act as an anti-conflict agent in this paradigm, alleviating the depressed performance in downshifted animals. As such, the negative contrast paradigm can be employed as a useful tool to probe for long-term effects of in utero alcohol exposure in mice. It will permit a biochemical correlate of a behavioral task which is "frustrating" and permit an evaluation of the anxiolytic properties of ethanol as a function of prenatal alcohol exposure. Thus, these studies will examine the behavioral, pharmacological, and neuroendocrinological ramification of prenatal alcohol exposure in mice using a single test paradigm. These issues are of clinical importance and, therefore, of interest to examine in an animal model with the ultimate goal of generating data of significance to children with Fetal Alcohol Syndrome.