We previously showed the prenatal alcohol exposure (PAE) induced precocious growth of E15.5 internal capsule axons. We set out to further delineate which axon tracts were affected and a potential mechanism for this phenomenon. Pregnant Swiss Webster mice were exposed to saline or 20% ethanol via subcutaneous injection from embryonic days (E) 7.5 until E14.5. E15.5 embryos were captured via C-section and brains were either fixed for immunostaining or flash frozen for tissue punches. To identify internal capsule axons we performed immunohistochemistry using L1 antibody to visualize all internal capsule axons and NetrinG1 antibody to identify thalamocortical axons specifically. mRNA was extracted from tissue punches to visualize Slit1, Robo1, Slit2, and Robo2 gene expression levels via real time RT PCR. We found that L1-expressing axons exhibited increased axon crossing in females with the opposite effect in males and no difference in Netrin-G1-expressing axons. We also found PAE increased Robo1 mRNA. Taken together, our results indicate that PAE elicits specific effects on axon trajectories, potentially via the Slit/Robo guidance family of repellents and receptors. These findings add to the growing body of evidence demonstrating alcohol disruptions of axon growth and guidance during embryonic development that may contribute to connectivity errors that characterize Fetal Alcohol Spectrum Disorders.