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Effect of cocaine, ethanol or nicotine on ornithine decarboxylase activity in early chick embryo brain
K Beeker1, C Smith, S Pennington
1Department of Biochemistry, East Carolina University School of Medicine, Greenville, NC 27834.
Abstract:
Fetal drug exposure causes multiple deficits in the developing child. For both humans and animal models, the single most common drug-related problem is fetal growth suppression. This defect is associated with significant perinatal morbidity and mortality and may also be related to significant behavioral problems appearing later in life. Studies focussed on the molecular mechanism of fetal drug effects in placental models are complicated by multiple interactions of the drug with mother, placenta and fetus. Using early (76-168 h) chick embryos as a non-placental model, and three common drugs of abuse (nicotine, ethanol and cocaine) it was found that each drug suppressed the peak in fetal brain ornithine decarboxylase (ODC) activity that normally occurs at 120 h of development. For each drug, the decrease in ODC activity at 120 h was followed by a small but significant increase in ODC. Thus, although the drug-treated embryos were smaller in size, they appeared to be undergoing compensatory growth and, in fact, became equal in weight to the vehicle-treated animals, if allowed to hatch.
Insights
Fetal exposure to nicotine, ethanol, and cocaine suppresses early brain development. Despite initial growth suppression, chick embryos showed compensatory growth, reaching normal weights by hatching.
Area of Science:
- Developmental biology
- Pharmacology
- Toxicology
Background:
- Fetal drug exposure is a leading cause of developmental deficits, particularly fetal growth suppression.
- This growth suppression is linked to perinatal complications and later-life behavioral issues.
- Placental models complicate studying drug effects due to complex mother-placenta-fetus interactions.
Purpose of the Study:
- To investigate the molecular mechanisms of fetal drug effects using a non-placental model.
- To examine the impact of common drugs of abuse on early embryonic development and ornithine decarboxylase (ODC) activity.
Main Methods:
- Utilized early chick embryos (76-168 hours) as a non-placental model for drug exposure studies.
- Administered nicotine, ethanol, and cocaine to assess their effects on fetal brain ornithine decarboxylase (ODC) activity.
- Monitored embryonic growth and weight changes in response to drug treatment.
Main Results:
- Each tested drug (nicotine, ethanol, cocaine) suppressed the normal peak in fetal brain ornithine decarboxylase (ODC) activity at 120 hours.
- Following the suppression, a small but significant increase in ODC activity was observed for all drug-treated groups.
- Drug-exposed embryos, initially smaller, exhibited compensatory growth and achieved equal weight to controls by hatching.
Conclusions:
- Early embryonic exposure to common drugs of abuse disrupts key developmental processes, including ODC activity.
- The chick embryo model effectively demonstrates drug-induced developmental alterations without placental confounding factors.
- Observed compensatory growth suggests potential resilience or adaptive mechanisms in embryonic development following drug exposure.