Effects of early in ovo administration of ethanol on expression of the GABAergic neuronal phenotype in the chick embryo.

In order to study the influence of ethanol on GABAergic neuronal expression in the chick embryonic brain, activity of glutamate decarboxylase (GAD; a GABAergic neuronal marker) was examined in whole brain derived from embryonic chick following the in ovo administration of ethanol. GAD activity was already detectable by 3 days of embryogenesis and exhibited a logarithmic increase up to embryonic day 16 (E16). By E18, GAD activity began to plateau. Administration of ethanol (10 mg/50 microliters/day) to embryos in ovo on days E1-E3, resulted in increased GAD activity in whole brain when embryos were sacrificed at E8. However, when embryos were administered ethanol on days E4-E7, activity of GAD was unchanged as compared with controls. Similarly, when embryos were administered ethanol chronically from E1-E7 no significant effect was observed in GAD activity. The increase observed in GAD activity after exposure to ethanol during a period of active neuronal proliferation (E1-E3) supports our view that E1-E3 is the critical period of sensitivity to ethanol with respect to the development of neuronal phenotypes during embryogenesis. Furthermore, the absence of any significant effect of ethanol administered from E1 to E7 on GAD activity suggests the existence of a compensatory response to ethanol insult.