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Fetal alcohol spectrum disorder, caused by maternal alcohol consumption, can cause a variety of symptoms, including deficits in sensory or motor processing. To identify possible causes of these deficits, we focused on the migration of thalamocortical axons (TCAs) during development. TCAs pass sensory information from the thalamus to the cortex. TCAs require cues for proper migration, including a cell population known as corridor cells. Corridor cells guide TCAs through a nonpermissive region of the brain, the medial ganglionic eminence (MGE). Corridor cells are born in the lateral ganglionic eminence and migrate to the MGE from embryonic days (E) 11.5 to E13.5. We measured the number of E12.5-born cells in the MGE at E14.5 using bromodeoxyuridine (BrdU)-birth dating. We marked cells in embryonic mice by injecting pregnant dams with BrdU at E12.5. BrdU-birth dating labels the progeny of all cells reproducing at the time of injection, including corridor cells. This allows us to measure differences in proliferation caused by alcohol exposure. We performed immunostaining to visualize BrdU-positive cells in the MGE at E14.5. We captured images of the MGE and counted BrdU-positive cells using ImageJ software. We found no significant difference in the number of BrdU-positive cells in the MGE of control and ethanol-exposed brains. Although the number of cells in the MGE was unchanged, alcohol may affect corridor cells in other ways. BrdU-birth dating labels cells at only one time, although alcohol can affect cells at any time. We will consider different times and corridor cell distribution in future work.
Sicher, Avery, "Number of E12.5-born BrdU-labeled Cells in the Medial Ganglionic Eminence is Unaffected by Prenatal Alcohol" (2018). Biology Summer Fellows. 61.