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Fetal alcohol exposure poses a significant social problem. Conservative rates of Fetal alcohol syndrome and Alcohol-Related Neurodevelopmental Disorders (ARND) together have been estimated at 9.1/1000 live births (Sampson 1997). Prenatal ethanol exposure can produce subtle learning disabilities in children, which may not become apparent until a child is school-aged and can occur in the absence of other physical evidence of alcohol-related birth defects. Along with cognitive deficits, ARND has been associated with an increased risk of psychiatric disorders such as Major Depressive Disorder (MDD). Major Depressive Disorder (MDD) has been linked to polymorphisms in the Brian Derived Neurotrophic Factor (BDNF) gene and patients with MDD have low serum BDNF levels (Levinson 2005, Chen et al 2001). Also post-mortem depressed patients who were on anti-depressant drugs have shown increased levels of BDNF (Chen et al 2001). BDNF given to stressed animals can even produce an antidepressant-like effect through the antagonism of a model of depression called learned helplessness behavior (Karege 2002). Efforts to better understand how prenatal ethanol increases susceptibility to MDD and the mechanism(s) by which ethanol produces these defects will rely on the study of these effects in animal models of prenatal ethanol exposure. Recently, our laboratory developed a mouse Fetal Alcohol Exposure (FAE) model which displays neurochemical and learning deficits. This model was used to explore the relationship of FAE-induced learned helplessness and changes in BDNF in the adult brain. Prenatal alcohol exposure was shown to produce an increase in learned helplessness and this was associated with a decrease in BDNF levels in the brain. These findings support the hypothesis that ARND is associated with an increase in depressive behavior and that lower levels of BDNF following prenatal exposure to alcohol may be involved.