Hoff S F
Department of Pharmacology, University of Health Sciences, Chicago Medical School, IL 60064.
Brain Res Bull. 1988 Jul;21(1):47-54. doi: 10.1016/0361-9230(88)90119-0.
In animal models of Fetal Alcohol Syndrome, ethanol causes a number of changes in brain development, with many of these changes being very transient. This is especially true for the process of synaptogenesis in different brain areas. Our quantitative electron microscopic study of synaptogenesis in the molecular layer of the rat dentate gyrus supports the above statement, by demonstrating that ethanol has no effect on the appearance of synapses in the dentate gyrus during early postnatal life (10-30 days old). However, prenatal ethanol exposure does appear to affect the process of synapse turnover, which is indicated by the significantly delayed appearance of complex (curved) synapses and multiple synaptic contacts on single axonal terminals. Efficient synapse turnover is thought to be required for the normal maintenance of neuronal plasticity, which in turn ensures an animal's ability to respond to novel environments, tasks and injuries. It would seem that the prenatal neurotoxicology of ethanol may manifest itself by more subtle mechanisms at sites of structural and functional importance.
在胎儿酒精综合征的动物模型中，乙醇会导致大脑发育出现多种变化，其中许多变化非常短暂。不同脑区的突触形成过程尤其如此。我们对大鼠齿状回分子层突触形成进行的定量电子显微镜研究支持了上述说法，研究表明，乙醇对出生后早期（10 - 30天大）齿状回中突触的出现没有影响。然而，产前乙醇暴露似乎确实会影响突触更新过程，这表现为复杂（弯曲）突触和单个轴突终末上多个突触接触的出现显著延迟。有效的突触更新被认为是神经元可塑性正常维持所必需的，而神经元可塑性又确保了动物对新环境、任务和损伤作出反应的能力。乙醇的产前神经毒理学似乎可能通过在结构和功能重要部位的更细微机制表现出来。
