Swanson D J, King M A, Walker D W, Heaton M B
Department of Neuroscience, University of Florida Brain Institute, University of Florida College of Medicine, Gainesville 32610-0244, USA.
Alcohol Clin Exp Res. 1995 Oct;19(5):1252-60. doi: 10.1111/j.1530-0277.1995.tb01608.x.
In animal models of fetal alcohol syndrome (FAS), the hippocampus has been shown to be especially sensitive to the effects of prenatal ethanol exposure, exhibiting neuronal loss and alterations in neuritic process elaboration. We have characterized the influence of chronic prenatal ethanol treatment (CPET) on the postnatal expression of choline acetyltransferase (ChAT) in the hippocampus and the septal area that contains neurons that provide the primary cholinergic innervation to the hippocampus. On gestation days 1-22, pregnant rats were either fed an ethanol-containing liquid diet, pair-fed a calorically equivalent sucrose-containing diet, or given rat chow ad libitum. In Chow control animals, the ontogenetic progression of ChAT activity in the septal area and hippocampus was characterized by a significant period of upregulation during the 2nd and 3rd postnatal weeks, exhibiting and an approximate 5-fold increase (septal area) and 7-fold increase (hippocampus) by postnatal day 21 (P21). At P14, ethanol exposure reduced septal and hippocampal ChAT activity levels, compared with those of pair-fed offspring. ChAT activity reached control levels by P21 in ethanol-exposed pups, suggesting that the earlier decline in activity may reflect a delay in the ontogenetic upregulation. In addition, there was a trend toward increased septal and hippocampal ChAT activities at P1 and P7 in both liquid diet groups. This liquid diet-stimulated increase may mask the effects of ethanol on early postnatal ChAT expression in the septohippocampal system. The results suggest that prenatal ethanol exposure may influence factors that regulate the developmental expression of ChAT in the septohippocampal system.(ABSTRACT TRUNCATED AT 250 WORDS)
在胎儿酒精综合征（FAS）的动物模型中，海马体已被证明对产前乙醇暴露的影响特别敏感，表现出神经元丢失和神经突发育过程的改变。我们已经描述了慢性产前乙醇处理（CPET）对海马体和隔区中胆碱乙酰转移酶（ChAT）产后表达的影响，隔区含有为海马体提供主要胆碱能神经支配的神经元。在妊娠第1至22天，给怀孕大鼠喂食含乙醇的液体饮食、配对喂食热量相当的含蔗糖饮食或随意给予大鼠食物。在正常饮食对照组动物中，隔区和海马体中ChAT活性的个体发育进程的特点是在出生后第2周和第3周有一个显著的上调期，到出生后第21天（P21）时，隔区ChAT活性增加约5倍，海马体增加约7倍。在P14时，与配对喂食的后代相比，乙醇暴露降低了隔区和海马体的ChAT活性水平。在乙醇暴露的幼崽中，ChAT活性在P21时达到对照水平，这表明早期活性下降可能反映了个体发育上调的延迟。此外，两个液体饮食组在P1和P7时隔区和海马体的ChAT活性都有增加的趋势。这种液体饮食刺激的增加可能掩盖了乙醇对隔海马系统产后早期ChAT表达的影响。结果表明，产前乙醇暴露可能会影响调节隔海马系统中ChAT发育表达的因素。（摘要截短至250字）
