Journal
NEUROSCIENCE
Volume 181, Issue -, Pages 196-205Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2011.02.059
Keywords
nrsf conditional knockout; ethanol; apoptosis; caspase-3; fetal alcohol syndrome
Categories
Funding
- National Natural Science Foundation of China [30670438, 30770659, 90919004]
- National 863 project [2008AA02Z126]
- National Key Project [2010CB945501]
- Science and Technology Commission of Shanghai Municipality [06DZ19004]
- E-Institutes of Shanghai Municipal Education Commission [E03003]
- Program for NCET
Ask authors/readers for more resources
The transcription regulator, neuron-restrictive silencer factor (NRSF), also known as repressor element-1 silencing transcription factor (REST), plays an important role in neurogenesis and various neuronal diseases such as ischaemia, epilepsy, and Huntington's disease. In these disease processes, neuronal loss is associated with abnormal expression and/or localization of NRSF. Previous studies have demonstrated that NRSF regulates the effect of ethanol on neuronal cells in vitro, however, the role of NRSF in ethanol-induced neuronal cell death remains unclear. We generated nrsf conditional knockout mice using the Cre-IoxP system to disrupt neuronal expression of nrsf and its truncated forms. At postnatal day 6, ethanol significantly increased the expression of REST4, a neuron-specific truncated form of NRSF, in the brains of wild type mice, and this effect was diminished in nrsf conditional knockout mice. The apoptotic effect of ethanol was pronounced in multiple brain regions of nrsf conditional mutant mice. These results indicate that NRSF, specifically REST4, may protect the developing brain from ethanol, and provide new evidence that NRSF can be a therapeutic target in foetal alcohol syndrome (FAS). (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available