Early in ovo exposure of chick embryos to ethanol prevents the neuronotrophic effects of intracerebral NGF administration on cholinergic phenotypic expression.

We have reported that ethanol administration during early neuroembryogenesis significantly alters neuronal phenotypic expression. In addition, previous findings have indicated that ethanol may interfere with the neurotrophic effects of NGF. In this study, we examined the cholinergic neuronal response to NGF given intracerebrally to embryos at embryonic day 8 (E8) which were exposed to ethanol in ovo via the air sac at E1-3. We found that doses of NGF ranging from 0.01 to 1 ng/2 microliters/embryo given intracerebrally to untreated embryos at E8, and sacrificed at E10, significantly increased choline acetyltransferase (ChAT) activity, the marker for cholinergic neuronal expression. This response was most marked in spinal cord as compared with the low response observed in cerebral hemispheres. In control embryos treated with saline at E1-3 and then receiving NGF intracerebrally at E8, ChAT activity in the spinal cord increased with increasing NGF doses; the highest value was obtained with 0.1 ng NGF. In contrast, in ethanol-treated embryos, ChAT activity was not affected by intracerebral administration of NGF and, in fact, the highest dose (0.1 ng) produced a decrease in ChAT activity. We conclude that: (1) intracerebral administration of NGF produces differential cholinotrophic effects in the embryonic chick CNS; and (2) exposure to ethanol during early neuroembryogenesis interferes with the cholinotrophic effects of NGF.