Alcohol-induced neuroapoptosis in the fetal macaque brain

NEUROBIOLOGY OF DISEASE

卷:40

Article

Farber, Nuri B.¹  Creeley, Catherine E.¹  Olney, John W.¹ 

[1] Washington Univ, Dept Psychiat, St Louis, MO 63110 USA

关键词: Ethanol;    Alcohol;    Macaque;    Apoptosis;    Caspase-3;    Fetal alcohol syndrome;    Fetal alcohol spectrum disorder;    Non-human primate;    Schizophrenia;    Bipolar disorder;   

DOI  :  10.1016/j.nbd.2010.05.025

来源: Elsevier

【 摘 要 】

The ability of brief exposure to alcohol to cause widespread neuroapoptosis in the developing rodent brain and subsequent long-term neurocognitive deficits has been proposed as a mechanism underlying the neurobehavioral deficits seen in fetal alcohol spectrum disorder (FASD). It is unknown whether brief exposure to alcohol causes apoptosis in the fetal primate brain. Pregnant fascicularis macaques at various stages of gestation (G105 to G155) were exposed to alcohol for 8 h, then the fetuses were delivered by caesarian section and their brains perfused with fixative and evaluated for apoptosis. Compared to saline control brains, the ethanol-exposed brains displayed a pattern of neuroapoptosis that was widespread and similar to that caused by alcohol in infant rodent brain. The observed increase in apoptosis was on the order of 60-fold. We propose that the apoptogenic action of alcohol could explain many of the neuropathological changes and long-term neuropsychiatric disturbances associated with human FASD. (C) 2010 Elsevier Inc. All rights reserved.

【 授权许可】

Free