of brain weight, neuron loss, hyperactivity, learning deficits, deficiencies in memory function, and perseverative tendencies. These results encourage the further use of this animal model of FAS, particularly to specify better the relationship between alcohol-induced brain damage and behavioral dysfunction. In addition, the model affords the potential to evaluate CNS disruption that is less extreme than cell loss, which may have important implications for lower levels of prenatal alcohol exposure in humans that do not lead to a diagnosis of FAS, but which nevertheless may have adverse effects on the development of the nervous system.
We thank Craig Pleggenkuhle and Bob Halloran for contributing to the behavioral testing, Blake Hamann for assisting with the cell counts, and Sara Hulsether, Jolonda Mahoney, and John Nichols for assisting with the artificial rearing. We also thank Keith Miller for constructing the radial maze.
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