Selective Direct Toxicity of Cocaine on Fetal Mouse Neurons: Teratogenic Implications of Neurite and Apoptotic
Marie-Cécile Nassogne1, Philippe Evrard1, Pierre J Courtoy1
1Cell Biology Unit, Christian de Duve Institute of Cellular Pathology, 75, avenue Hippocrate, B-1200 Brussels, BelgiumService de Neurologie Pédiatrique, Saint Luc Hospital, University of Louvain Medical School, B-1200 Brussels, Belgium.
Abstract:
This chapter reviews epidemiologic clinical surveys and experimental animal studies, indicating that cocaine may induce severe teratogenic effects on the developing brain. Evidence for direct toxic effects is next presented. Using cocultures of embryonic brain cells, we demonstrate that cocaine selectively affects neuronal cells, first causing a dramatic reduction in the number and length of neurites, then extensive neuronal death by apoptosis. By contrast, cocaine affected neither the abundance of astroglial cells nor their glial fibrillary acidic protein content. These effects are not due to cocaine metabolites. The contributions of indirect and direct effects that could account for cocaine neuroteratogenicity are finally discussed.
Insights
Cocaine exposure during development can harm the brain, causing significant neuronal cell death. These findings highlight the direct toxic impact of cocaine on developing neural cells.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Cocaine use during pregnancy is a significant public health concern.
- Epidemiologic and animal studies suggest potential teratogenic effects of cocaine on the developing brain.
Purpose of the Study:
- To investigate the direct toxic effects of cocaine on embryonic brain cells.
- To elucidate the mechanisms underlying cocaine-induced neuroteratogenicity.
Main Methods:
- Utilized cocultures of embryonic brain cells to assess cocaine's impact.
- Examined effects on neuronal and astroglial cell populations.
- Analyzed neurite outgrowth, cell viability, and apoptosis.
Main Results:
- Cocaine selectively induced significant reduction in neuronal cell neurite number and length.
- Cocaine exposure led to extensive neuronal death via apoptosis.
- Cocaine did not affect astroglial cell abundance or glial fibrillary acidic protein content.
- Observed effects were not attributable to cocaine metabolites.
Conclusions:
- Cocaine exerts direct toxic effects on developing neuronal cells.
- Apoptosis is a key mechanism in cocaine-induced neuroteratogenicity.
- Understanding these direct effects is crucial for addressing prenatal cocaine exposure.
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