Abstract
Rats exposed to ethanol in utero were assessed for changes in gait at 55 days of age. Ethanol-exposed animals had significantly shorter stride lengths, more open step angles, and less gait symmetry than control rats. There were no differences in stance width or apparent speed. This pattern of changes in motor function indicates that prenatal exposure to ethanol produces long-lasting “ataxia” in rats. These results closely resemble previous findings of altered gait following neonatal ethanol exposure in rats, as well as clinical findings in some FAS children. The results are consistent with an hypothesis of prenatal ethanol-induced disruption of functional hippocampal and/or cerebellar development. Ataxia and gait dysfunction may be sensitive indicators of ethanol teratogenesis.
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