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SELECTIVE VULNERABILITY OF EMBRYONIC CELL POPULATIONS TO ETHANOL-INDUCED APOPTOSIS: IMPLICATIONS FOR ALCOHOL RELATED BIRTH DEFECTS AND NEURODEVELOPMENTAL DISORDER
Citation:
Dunty, W. C., S. Y. Chen, R M. Zucker, D. B. Dehart, AND K. K. Sulik. SELECTIVE VULNERABILITY OF EMBRYONIC CELL POPULATIONS TO ETHANOL-INDUCED APOPTOSIS: IMPLICATIONS FOR ALCOHOL RELATED BIRTH DEFECTS AND NEURODEVELOPMENTAL DISORDER. ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH 25(10):1523-1535, (2001).
Description:
The locations of cell death and resulting malformations in embryos following teratogen exposure vary depending on the teratogen used, the genotype of the conceptus, and the developmental stage of the embryo at time of exposure. To date, ethanol-induced cell death has been characterized in very few stages of embryogenesis. The current investigation helps to fill this void by comprehensively mapping patterns of both programmed and ethanol-induced cell death in the central nervous system (CNS) and craniofacial region at 0.5 day intervals from gestational day (GD) 6.5-11 in mice. Normal programmed cell death (PCD) in control embryos was noted in the prechordal plate region at GD 8, the neuroepithelium of the fourth ventricle and anterior neuropore at GD 9, and within the ganglia of cranial nerves V, VII-VIII, IX, and X at GD 10. Acute maternal ethanol administration (2.9 g/kg) twelve hours prior to examination resulted in a dramatic increase in apoptosis within sites of PCD in the embryo. Moreover, ethanol-exposed specimens exhibited stage-dependant excessive cell death in other distinct cell populations, particularly within the developing CNS. Ethanol-induced apoptosis was notable as follows: GD 7.5-neuroectoderm; GD 8-neural plate and primitive streak; GD 9-alar plate and presumptive neural crest of the rostral hindbrain, especially at the mesencephalon/rhombencephalon junction; GD 9.5-10-branchial arches and rhombomeres; and GD 11-diencephalon, basal ganglia, pons, and developing cerebellum. The results of this study revealed developmental stage-specific cell populations/regions that are vulnerable to ethanol-induced apoptosis and provide new insight relative to the genesis of alcohol-related birth defects.