Moderate prenatal ethanol exposure increases total length of L1 axons in E15.5 mice

Abstract

Public health campaigns broadcast the link between heavy alcohol consumption during pregnancy and physical, cognitive, and behavioral birth defects; however, they appear less effective in deterring moderate consumption prevalent in women who are pregnant or of childbearing age. The incidence of mild Fetal Alcohol Spectrum Disorders (FASD) is likely underestimated because the affected individuals lack physical signs such as retarded growth and facial dysmorphology and cognitive/behavioral deficits are not commonly detected until late childhood. Sensory information processing is distorted in FASD, but alcohol effects on the development of axons that mediate these functions are not widely investigated. We hypothesize that alcohol exposure alters axon growth and guidance contributing to the aberrant connectivity that is a hallmark of FASD. To test this, we administered alcohol to pregnant dams from embryonic day (E) 7.5 to 14.5, during the time that axons which form the major forebrain tracts are growing. We found that moderate alcohol exposure had no effect on body weight of E15.5 embryos, but significantly increased the length of L1+ axons. Our findings support our hypothesis. Future studies will investigate cellular, molecular, and functional mechanisms that underlie these effects.