Young Chainllie, Olney John W
Department of Psychiatry, Washington University School of Medicine, 660 South Euclid, St. Louis, MO 63110, USA.
Neurobiol Dis. 2006 Jun;22(3):548-54. doi: 10.1016/j.nbd.2005.12.015. Epub 2006 Feb 3.
Exposure of infant rats or mice to ethanol on a single occasion during the period of rapid synaptogenesis can cause extensive apoptotic neurodegeneration throughout the developing CNS. Prior studies were designed to assess the effects of large doses of ethanol (comparable to heavy binge drinking), whereas in the present study, we sought to determine what magnitude and duration of blood ethanol elevation are required to trigger a minimal neuroapoptotic response. We found that a rise in blood ethanol to a level in the range of 50 mg/dl for a duration of 30 to 45 min was sufficient to trigger a significant neuroapoptosis response deleting approximately 20,000 neurons per infant mouse brain. Since blood ethanol elevations in this range are commonly achieved by humans in a social drinking context, a mother with only a moderate drinking habit might expose her fetus to such elevations on multiple occasions during pregnancy.
在快速突触发生期，新生大鼠或小鼠单次接触乙醇可导致整个发育中的中枢神经系统广泛的凋亡性神经退行性变。先前的研究旨在评估大剂量乙醇（相当于重度暴饮）的影响，而在本研究中，我们试图确定血液乙醇浓度升高到何种程度以及持续多长时间才能引发最小的神经凋亡反应。我们发现，血液乙醇浓度升高至50mg/dl并持续30至45分钟，足以引发显著的神经凋亡反应，每只新生小鼠大脑中约有20,000个神经元被清除。由于在社交饮酒情况下，人类通常会使血液乙醇浓度升高到这个范围，因此仅有适度饮酒习惯的母亲在怀孕期间可能会多次使胎儿暴露于这样的乙醇浓度升高情况。
