Bcl-2 overexpression protects the neonatal cerebellum from ethanol neurotoxicity
| Autor: | Marieta B. Heaton, D. Blaine Moore, Michael Paiva, Theresa Gibbs, Ora Bernard |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Genetically modified mouse
Cerebellum medicine.medical_specialty Programmed cell death Neurotoxins Central nervous system Fetal alcohol syndrome Cell Count Mice Transgenic Biology Neuroprotection Mice Purkinje Cells Internal medicine medicine Animals Molecular Biology Analysis of Variance Ethanol General Neuroscience Neurotoxicity Gene Expression Regulation Developmental medicine.disease Genes bcl-2 Mice Inbred C57BL medicine.anatomical_structure Endocrinology Animals Newborn Fetal Alcohol Spectrum Disorders Apoptosis Immunology Neurology (clinical) Developmental Biology |
| Zdroj: | Brain Research. 817:13-18 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/s0006-8993(98)01173-1 |
| Popis: | 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 P5, 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. |
| Databáze: | OpenAIRE |
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