Ethanol Blocks Proliferation Of Nueral Reogenitors And Effects On The Signaling Pathways

1. backgroundPrenatal alcohol exposure is the leading known cause of mental retardation. Children with fetal alcohol syndrome have significantly smaller brain size and thinner cerebral cortex than normal, resulting from decreases in the total number of cells. We have expanded neuroepithelial cells dissociated from the embryonic rat telencephalon in serum-free defined medium containing bFGF in order to generate a model neuroepithelium to study the interaction of ethanol with growth factor-stimulated proliferation. The model can help us to understand the mechanism of the loss of CNS caused by alcohol. Otherwise, it can provide scientific foundation for treating prenatal alcohol exposure. It was reported neural stem cells were planted in adherent culture. The new method contribute to study the effect that ethanol blocked proliferation, such as cell counting and fluorescent dying.In the pictures of neurospheres ultrastructure, gap junction was found on the borders of two neighbor cells. Gap junction plays a important role during proliferation, differentiation, development, location and maintaining configuration of neural cells. Gap junction is a special protein channel, made up by protein molecule called connexin or connexon. Connexins are a multigenic family of proteins that can be distinguished on the basis of their molecular weight. It is important to assure the type of connexon for studying forming neurospheres and proliferation and differentiation of neural cells in CNS.It was reported that during differentiation neural progenitor cells secreted some foctor that could restrain proliferation of glioma. Our initial study of the...