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Ethanol exposure affects trophic factor activity and responsiveness in chick embryo
M B Heaton1, D J Swanson, M Paiva
1Department of Neuroscience, University of Florida College of Medicine, Gainesville 32610-0244.
Alcohol (Fayetteville, N.Y.)
|March 1, 1992
Summary
Prenatal ethanol exposure significantly reduced neurotrophic activity in chick embryos, impacting neuronal survival and development. This suggests ethanol may alter brain development, potentially contributing to fetal alcohol syndrome anomalies.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Chronic prenatal ethanol exposure is a known teratogen.
- Fetal Alcohol Syndrome (FAS) is associated with central nervous system (CNS) anomalies.
- Neurotrophic factors are crucial for neuronal survival and development.
Purpose of the Study:
- To investigate the effects of chronic prenatal ethanol exposure on neurotrophic activity in chick embryos.
- To determine if ethanol exposure alters the neurotrophic content and responsiveness of forebrain extracts.
- To examine the impact on dorsal root ganglia (DRG) viability and neurite outgrowth.
Main Methods:
- Chick embryos were exposed to ethanol or saline from embryonic day 4 (E4) to E13.
- Forebrain extracts (FBX) were prepared from E16 embryos.
- Cultured dorsal root ganglia (DRG) were treated with FBX and nerve growth factor (NGF).
- Neuronal survival and process elaboration were assessed.
Main Results:
- Ethanol-treated embryos showed significantly reduced neurotrophic activity in FBX compared to controls.
- Ethanol exposure impaired DRG viability in the presence of NGF.
- While DRG survival was unaffected by FBX from ethanol-treated embryos, neurite production was significantly reduced.
Conclusions:
- Chronic prenatal ethanol exposure alters neurotrophic factor content and neuronal responsiveness.
- These alterations may contribute to the CNS anomalies observed in fetal alcohol syndrome.
- The study highlights potential mechanisms underlying ethanol's neurodevelopmental toxicity.