Alcohol and Alcoholism Advance Access published online on May 30, 2007
Alcohol and Alcoholism, doi:10.1093/alcalc/agm032
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The Author 2007. Published by Oxford University Press on behalf of the Medical Council on Alcohol.
Prenatal Alcohol Exposure and the Neuroapoptosis with Long-Term Effect in Visual Cortex of Mice
Institute of Neurobiology, Henan University, Jinming Campus of Henan University, Kaifeng 475004, Henan Province, P. R. China
* Author to whom correspondence should be addressed at: Institute of Neurobiology, Henan University, Jinming Campus of Henan University, Kaifeng 475004, Henan Province, P. R. China. Tel: 86-378-3880292; Fax: 86-378-3880585; E-mail: jinbo_deng{at}henu.edu.cn
Received 4 January 2007; first review notified 15 February 2007; in revised form 24 February 2007; accepted 6 March 2007
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Abstract |
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Aims: The prenatal ethanol exposure induced neuroapoptosis and neuron loss in visual cortex would be investigated in mice at P0, P7 and P14. Methods: Intubating pregnant mice ethanol daily began on E5 and continued through the pup's birth. The neuroapoptosis in visual cortex was visualized by the caspase 3 immunocytochemistry, and the neuron loss was observed with Nissl method as well. Results: With prenatal ethanol exposure, the dose-dependent neuroapoptosis and neuron loss in visual cortex could be found at P0 and even at P7 and P14 as well. Conclusions: The prenatal ethanol exposure induced neuroapoptosis and neuron loss will persist into postnatal stage, and the long-term effect of neuroapoptosis might be one of the causes of postnatal neurobehavioural disturbances associated with fetal alcohol syndrome.