Gohlke J M, Griffith W C, Bartell S M, Lewandowski T A, Faustman E M
Institute for Risk Analysis and Risk Communication, Department of Environmental Health, University of Washington, Seattle, Wash 98105-6099, USA.
Dev Neurosci. 2002;24(6):467-77. doi: 10.1159/000069357.
We have developed a computational model that allows for the evaluation of normal and perturbed neurodevelopmental processes. This mathematical construct is used to test the hypothesis that reduced neuronal production is the critical mechanism behind fetal alcohol syndrome. Model predictions of normal neurodevelopment match independent stereological measures but challenge estimates generated using a previously published model of normal neocortical neuronogenesis. Evaluation of data showing an increased cell cycle length after prenatal exposure to ethanol during neocortical neuronogenesis yields predictions of cellular deficits that can account for the permanent neocortical neuronal loss seen in rodents exposed to ethanol concentrations of public health relevance.
我们开发了一种计算模型，可用于评估正常和受干扰的神经发育过程。这个数学结构用于检验以下假设：神经元生成减少是胎儿酒精综合征背后的关键机制。正常神经发育的模型预测与独立的立体测量结果相符，但对使用先前发表的正常新皮质神经发生模型生成的估计提出了挑战。对新皮质神经发生期间产前暴露于乙醇后细胞周期长度增加的数据进行评估，得出了细胞缺陷的预测结果，这些结果可以解释在暴露于具有公共卫生相关性乙醇浓度的啮齿动物中看到的永久性新皮质神经元损失。
