Institution: Ursinus College, Collegeville, Pennsylvania 19426
Abstract: Fetal Alcohol Spectrum Disorders (FASD) is the label given to birth defects causing impairment in motor movement, behavior, cognition, and facial morphology to the fetus due to alcohol consumption during pregnancy. In animal studies, prenatal ethanol exposure was found to cause apoptosis of basal ganglia cells, causing a reduction in overall size. The basal ganglia are responsible for control of voluntary movements, cognition, procedural learning, among other functions. The decrease in size of the basal ganglia could relate to the motor impairment and cognitive problems that are observed as a phenotype of FASD. We are using a Drinking in the Dark (DID) paradigm to model FASD in mice and to mimic moderate human binge drinking. In this paradigm, for 2-4 hours during the dark period when mice are most active, tap water and a 20% ethanol solution were given to the control and experimental group respectively. An islet-1 antibody was used to label striatal cells within the area of the basal ganglia. We hypothesized that within the lateral ganglionic eminences (LGE), the location of developing striatum within the basal ganglia, that the number of islet-1 cells would decrease and there would be a difference in the distribution in the cells of embryonic day (E) 14 mice with prenatal ethanol exposure. The data suggests that the hypothesis was not supported and no significant difference between groups for islet-1 cell count or distribution of the cells within the LGE was found. This study suggests that there is no difference in striatal cell count, at this time in development, with prenatal ethanol consumption using the DID model in Swiss Webster mice.