Bcl-2 overexpression protects the neonatal cerebellum from ethanol neurotoxicity
- Author(s)
- Heaton, MB; Moore, DB; Paiva, M; Gibbs, T; Bernard, O;
- Details
- Publication Year 1999-01-30,Volume 817,Issue #1-2,Page 13-18
- Journal Title
- BRAIN RESEARCH
- Publication Type
- Journal Article
- Abstract
- The developing nervous system is extremely sensitive to ethanol, and exposure often produces a condition known as the fetal alcohol syndrome. Although mechanisms underlying developmental ethanol toxicity have long been sought, they remain poorly understood. In this study, we examined the ability of the cell death repressor gene bcl-2 to protect against ethanol neurotoxicity. Transgenic mice overexpressing bcl-2 in neurons were exposed to ethanol vapor on postnatal days 4 and 5, which is the peak period of vulnerability of cerebellar Purkinje cells to ethanol. While exposure of wild-type animals to ethanol resulted in significant loss of Purkinje cells by pi, similar exposure of homozygous and heterozygous transgenics had no effect on the number of these neurons. This study suggests that bcl-2 can protect neurons from ethanol neurotoxicity and that modulation of cell death effector or repressor gene products may play a significant role in developmental ethanol neurotoxicity. (C) 1999 Elsevier Science B.V. All rights reserved.
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- FETAL ALCOHOL SYNDROME; NERVE GROWTH-FACTOR; PURKINJE-CELL LOSS; RAT CEREBELLUM; CYTOCHROME-C; REGIONAL DIFFERENCES; TRANSGENIC MICE; BINGE EXPOSURE; NEURONAL LOSS; DEATH
- Publisher's Version
- https://doi.org/10.1016/S0006-8993(98)01173-1
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1999-01-30 12:00:00