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Fetal alcohol spectrum disorder (FASD) is an umbrella term used for alcohol-related disorders resulting from prenatal alcohol exposure (PAE). Such exposure can cause sensory and attention processing deficits, among other more severe symptoms. To study these deficits, we looked to the migration of thalamocortical axons (TCAs). TCAs transmit sensory information from the thalamus to the cortex, requiring guidance and assistance to cross the non-permissive medial ganglionic eminence (MGE). Guidepost cells referred to as corridor cells originate in the lateral ganglionic eminence (LGE) and form a bridge for TCAs in the MGE around embryonic (E) days 11.5 to 13.5. Interneurons are similar GABAergic neurons that increase in number with PAE and briefly overlap with corridor cells. We hypothesized a decrease in corridor cells within the MGE and an ethanol-blunting effect on sex difference. We studied embryos at E13.5, born from dams injected with either 15 µL/kg ethanol or saline from E6.5 onward, to analyze corridor cell count. Using immunohistochemistry, we stained for Islet1 nuclei in the MGE and photographed those sections on a compound microscope. With ImageJ software, we measured MGE area and calculated the average number of Islet1 nuclei per 1000 microns. There was no significant difference in cell count between ethanol- and saline-treated embryos. Previous studies have found differences in PAE behavior based on sex along with Favero lab findings of a blunting effect. Future work will include continued data analysis to expand the embryo sample size and further study of the ethanol-blunting effect related to sex.
Springmann, Paige, "Corridor Cell Count in Medial Ganglionic Eminence Unaltered by Prenatal Alcohol Exposure" (2019). Neuroscience Summer Fellows. 12.
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