Chick embryos were given daily injections of ethanol (approximately 30
mg/day) either chronically from embryonic days 4 to 15 (E4-E15) or E1
8, or acutely from E15 to E18. Untreated and saline-injected embryos s
erved as controls. Although morphological indicators of developmental
age were not different among groups, chronic ethanol reduced weights o
f several brain regions. Similar to rodent models of prenatal ethanol
exposure, chronic ethanol treatment reduced cerebellar Purkinje cell n
umbers compared to controls. Chronic but not acute ethanol exposure re
sulted in a significant reduction in choline acetyltransferase activit
y in the optic tectum (OT) and forebrain (FB) compared with controls.
This study demonstrates that the chick embryo is a viable model to inv
estigate the effects of ethanol exposure on CNS development. Unlike th
e mammalian fetus, the avian embryo is isolated from maternal interact
ions and may prove more useful in investigating the mechanisms by whic
h ethanol directly influences brain development.