Becker H C, Diaz-Granados J L, Randall C L
Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, USA.
Pharmacol Biochem Behav. 1996 Dec;55(4):501-13. doi: 10.1016/s0091-3057(96)00255-9.
The deleterious effects of prenatal ethanol exposure have been extensively documented in clinical and experimental studies. This paper provides an overview of work conducted with mice to examine the myriad of adverse consequences that result from embryonic/fetal exposure to ethanol. All of the hallmark features of the clinical fetal alcohol syndrome have been demonstrated in mice, including prenatal and postnatal growth retardation, structural malformations and behavioral abnormalities associated with central nervous system dysfunction. As expected, the severity and profile of effects is related to both dosage level and timing of exposure. In addition, these effects have been demonstrated following acute and chronic exposure, with a variety of routes of administration employed. Furthermore, a number of strains have been used in these studies and the variant response (susceptibility) to the teratogenic actions of ethanol exhibited among different mouse strains support the notion that genetic factors govern, at least in part, vulnerability to these effects of ethanol. More recent studies using mouse models have focused on examining potential mechanisms underlying the full spectrum of ethanol's teratogenic actions.
产前乙醇暴露的有害影响已在临床和实验研究中得到广泛记录。本文概述了对小鼠进行的研究工作,以探讨胚胎/胎儿暴露于乙醇所导致的众多不良后果。临床胎儿酒精综合征的所有标志性特征在小鼠中均已得到证实,包括产前和产后生长迟缓、结构畸形以及与中枢神经系统功能障碍相关的行为异常。正如预期的那样,效应的严重程度和特征与剂量水平和暴露时间均有关。此外,在急性和慢性暴露后,采用多种给药途径均已证实了这些效应。而且,这些研究中使用了多种品系,不同小鼠品系对乙醇致畸作用表现出的不同反应(易感性)支持了以下观点,即遗传因素至少在一定程度上决定了对乙醇这些效应的易感性。最近使用小鼠模型的研究集中于探究乙醇致畸作用全貌背后的潜在机制。