Low-dose prenatal alcohol exposure modulates weight gain and eliminates fractalkine expression in e14.5 mouse embryos

• Main Authors: Jordyn Karliner, Mark Nagy, Joyce Sanya, Noah Yeagley, Zoe Barnett-Ohori, Lauren D’Ortona, Jill Lawrence, R. Colin McNamara, Rachel Boas, Heather Brubaker, Spencer Collopy, Justin Nolan, Carlita Favero
• Format: Article
• Language: English
• Published: Appalachian State University Honors College 2017-07-01
• Series: Impulse: The Premier Undergraduate Neuroscience Journal
• Subjects: DiD; FASD; microglia
• Online Access: https://impulse.appstate.edu/sites/impulse.appstate.edu/files/Karliner%20et%20al.2017.pdf

Fetal Alcohol Spectrum Disorder (FASD) is caused by maternal alcohol consumption during pregnancy and often leads to long-lasting developmental symptoms, including increased microglial migration and increased release of the chemokine, fractalkine, both of which play a role in embryonic brain development. However, the effects of low-dose alcohol exposure on microglia and fractalkine embryonically are not well documented. This study addresses this gap by using the voluntary drinking paradigm, Drinking in the Dark (DiD), to expose mice to acute doses of alcohol from embryonic day 7.5 (E7.5) to E14.5. Maternal mice and embryo analyses revealed increased embryo weights and a trend of increased gestational weight gain in alcohol-exposed mice compared to water-exposed mice. After quantifying soluble fractalkine concentrations through Western Blots, results indicated decreased fractalkine in alcohol-exposed mice compared to water-exposed. Overall, our data suggest that exposure to low doses of alcohol inhibits fractalkine release, which may affect microglial function.