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Effects of 2-methoxyethanol on mouse neurulation
K K Terry1, D B Stedman, B Bolon
1Chemical Industry Institute of Toxicology, Research Triangle Park, North Carolina 27709, USA.
Teratology
|November 1, 1996
Summary
2-methoxyethanol (2-ME) exposure on gestation day 8 causes open neural tubes and increased cell death in developing mouse embryos. Some recovery occurs, but developmental delays and malformations like exencephaly persist.
Area of Science:
- Developmental toxicology
- Neuroscience
- Embryology
Background:
- 2-methoxyethanol (2-ME) is a known developmental toxicant causing exencephaly.
- Early morphological effects of 2-ME on neurulating embryos are not well-documented.
Purpose of the Study:
- Investigate the impact of 2-ME on cell death patterns in embryonic neural folds.
- Characterize early morphological consequences of 2-ME exposure on neurulating embryos.
Main Methods:
- Maternal mice were treated with 2-ME on gestation day 8.
- Embryos were examined at multiple time points for neural tube closure, growth, and cell death.
- Nile blue sulfate staining and histopathology were used to assess cell death.
Main Results:
- 2-ME exposure increased the incidence of open neural tubes at all examined time points.
- Excessive cell death was observed in the neural fold neuroepithelium, particularly at sites of nonclosure.
- Low-dose 2-ME inhibited embryonic growth and delayed brain maturation.
Conclusions:
- 2-ME exposure induces significant cell death in the neural folds, contributing to neural tube defects.
- A trend toward repair and catch-up growth may occur later in gestation.
- Enhanced cell death is associated with neural tube regions vulnerable to nonclosure.