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Kentroti, S. et al.

Neuronal plasticity in the developing chick brain: interaction of ethanol and neuropeptides.

We have examined the influence of ethanol on cholinergic and catecholaminergic neuronal expression in the chick embryonic brain using choline acetyltransferase (ChAT) and tyrosine hydroxylase ( TH) activities as respective neuronal markers. Ethanol (5-20 mg/50 microliters/day), administered to embryos in ovo from day 1 to 3 of development produced a dose-dependent decrease in ChAT activity while TH activity exhibited a dose-dependent increase when embryos were sacrificed on embryonic day 8. The optimal neurotoxic dose of ethanol following this paradigm was 15 mg/day and the LD50 was 17.5 mg/day for the 3 days. Subsequently, embryos were administered ethanol (15 mg) either alone or concomitantly with growth hormone-releasing hormone (GH-RH; 100 ng/50 microliters/day). Previous studies from this laboratory have demonstrated both potent cholinotropic and catecholaminotropic effects for this neuropeptide, results confirmed in this study. Co-administration of ethanol and GH-RH resulted in a significant increase in ChAT activity as compared to both saline- and ethanol-treated controls when examined on day 8 of embryonic growth. No additive effect was observed in TH activity following co-administration of ethanol and GH-RH. The findings from this study are interpreted to mean that GH-RH represents a potent secondary signal to undifferentiated neuroblasts which may lead to a restoration of the cholinergic neuronal population following neurotoxic insult by ethanol.[1]

References

Neuronal plasticity in the developing chick brain: interaction of ethanol and neuropeptides. Kentroti, S., Vernadakis, A. Brain Res. Dev. Brain Res. (1990) [Pubmed]

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