Effects of Alcohol Exposure on Chick Thalamic Development

Fetal Alcohol Spectrum Disorder (FASD) is a broad term used to label the range of ontogenetic defects that can occur when an individual is prenatally exposed to alcohol. Various studies have shown that prenatal exposure to alcohol (PEA) leads to craniofacial dysmorphology and neurological defects. Studies on model organisms such as mice, zebrafish, and chicks have shown that the craniofacial defects resulting from PEA are caused by down-regulation of Sonic hedgehog (shh) activity. Previous work in the laboratory hosting my project demonstrated that shh plays a critical role in the development of the thalamus. Based on these two observations, I hypothesize that PEA has an influence on thalamus development, and that this could cause the thalamus-specific neurological defects in FASD patients. In this project I have set out to explore how exposure to different levels of alcohol affects the development of the thalamus. To log the effects of PEA on thalamus development, I am using in situ hybridization for different molecular markers on chick embryos exposed to different doses of ethanol. The chick embryo is a readily accessible amniote model that can be easily exposed to different amounts of ethanol during different stages in development.  My results show that exposure to ethanol reduces the expression of TFAP2α, which is a marker of neural crest cells in developing embryos, and of NGN2, a marker of the glutamatergic domain of the thalamus. In contrast, ethanol exposure does not seem to affect the expression of either sonic hedgehog (shh) or NKX2.2, a transcription factor and direct target of shh signaling. The lack of an effect on both shh and NKX2.2 suggests that shh signaling is not the factor impacting the expression of NGN2 in the developing thalamus. Comparing the expression of shh and shh-dependent genes with different ethanol treatments, will help to link the defects associated with PEA and FASD with the formation of the thalamus.