Gene Expression Is Disrupted by Ethanol Exposure on Chick Embryonic Choroid Plexus

Alcohol is a well-known teratogenic agent that causes neurodevelopmental diseases, including fetal alcohol syndrome. Alcohol-induced brain changes such as neuronal cell death, decreased adult neurogenesis, low level of neurotrophic factors and vital nutrients were previously reported. The choroid plexus (CP) is a multifunctional tissue located in four ventricles of the brain and formed early during neural development. The CP play important roles in producing cerebrospinal fluid, supplying numerous neurotrophic factors and eliminating brain metabolites, supporting homeostasis of central nervous system (CNS) both pre and postnatally. Involvement of the CP in alcohol-induced brain damage is yet to be discovered. This study aimed to investigate effects of alcohol on the developing CP of the lateral ventricles of the chick embryonic brains. We started treatments of alcohol (10% v/v and 15% v/v) in ovo chick embryos at embryonic day 3 (E3) every 24 hours and the CP examined at E8 and E12. Ethanol exposure induced growth retardation of the CP at E8 and E12 (decrease in both length and size). We then found that the mRNA expression of Otx2, Emx1 and Emx2 were up-regulated by ethanol exposure, and E2f5 mRNA was reduced and Foxj1 mRNA was increased expression in the CP of alcohol-treated embryos was confirmed. Herein, the current study showed the first time that alcohol disrupt the CP development related genes might lead to abnormal and dysfunction of the developing CP during early brain development, suggesting a pharmaceutical target for prevention and treatments of neurodevelopmental diseases.