Fetal Alcohol Spectrum Disorders (FASD) effect an estimated 2% of the population, causing a range of symptoms: from craniofacial defects to inhibited cortical growth (May, et al., 2009; Murawski, et al., 2015). Impaired medial forebrain function apparent in FASD is associated with lifelong cognitive behavioral deficits, but these consequences may be avoided with early diagnosis and intervention (Streissguth, et al., 2004). Our goal is to identify early neurobehavioral abnormalities that persist into adulthood that could potentially serve as early indicators for FASD. Mouse models of prenatal ethanol exposure were developed using a voluntary drinking paradigm that introduced a sweetened ethanol solution to pregnant dams. Impulsive behavior was observed during juvenile and adult testing, where ethanol-exposed mice displayed more risk-taking behavior in situations that induced inhibition in control mice. In contrast, ethanol-exposed mice were over-cautious in scenarios in which control mice experienced less anxiety. Ultimately, we observed what appears to be a persistent failure to accurately gauge and respond to environmental stimuli. This trait is analogous to impaired sensorimotor gating, or the unconscious cognitive ability to filter out irrelevant and attend relevant stimuli, a distinctive symptom of FASD. Future studies are needed to further establish early FASD markers applicable to humans.
Lawrence, Jill M., "Persistent Neurobehavioral Traits in a Mouse Model of Prenatal Ethanol Exposure" (2017). Neuroscience Honors Papers. 7.
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Funding provided by the Ursinus College Biology and Neuroscience Departments, as well as Student Research and Creative Projects.