The effects of ethanol on a fetus are extensive, devastating, and often permanent. Depending upon the population, ethanol affects as many as 2-5% of all live births. The most profound effects of ethanol are on the nervous system. Gestational ethanol exposure causes behavioral changes such as hyperactivity, attention deficit hyperactivity disorder (ADHD), learning and memory deficits, alterations in social behavior, and mental retardation. Such behavioral changes can also be seen in animals exposed to ethanol in the prenatal period, thus they provide good models for examining the underpinnings of the changes. One system that is particularly important for both social behavior and ADHD is the somatosensory system. Blocking sensory information within this system is sufficient to negatively affect social behavior. Ethanol causes alterations in the structure and function of this area. We will test the hypothesis that exposure to ethanol during development that causes structural alterations in somatosensory cortex will negatively affect behavior (including social behavior) and alter the neurochemistry of this region. Further, we will test the hypothesis that supplementation with docosahexaenoic acid, an omega-3 fatty acid, in the postnatal period will reverse ethanol-induced deficits in behavior, neurochemistry, and brain structure.
The experiments we propose examine the effect of a common environmental teratogen, alcohol, on social behavior and on the structure of and chemistry in one of the brain areas that subserves this behavior. In addition to determining the effects of ethanol on behavior, brain chemistry, and brain structure, we will also investigate the effects of supplementation with an omega-3 fatty acid on all three outcomes. This provides a unique opportunity to determine the role of specific brain regions and systems in social behavior, as well as examine a simple dietary intervention that appears to be therapeutic.
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