Basavarajappa Balapal S
Division of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.
New York State Psychiatric Institute, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA.
Brain Sci. 2015 Oct 29;5(4):456-93. doi: 10.3390/brainsci5040456.
One of the unique features of prenatal alcohol exposure in humans is impaired cognitive and behavioral function resulting from damage to the central nervous system (CNS), which leads to a spectrum of impairments referred to as fetal alcohol spectrum disorder (FASD). Human FASD phenotypes can be reproduced in the rodent CNS following prenatal ethanol exposure. Several mechanisms are expected to contribute to the detrimental effects of prenatal alcohol exposure on the developing fetus, particularly in the developing CNS. These mechanisms may act simultaneously or consecutively and differ among a variety of cell types at specific developmental stages in particular brain regions. Studies have identified numerous potential mechanisms through which alcohol can act on the fetus. Among these mechanisms are increased oxidative stress, mitochondrial damage, interference with the activity of growth factors, glia cells, cell adhesion molecules, gene expression during CNS development and impaired function of signaling molecules involved in neuronal communication and circuit formation. These alcohol-induced deficits result in long-lasting abnormalities in neuronal plasticity and learning and memory and can explain many of the neurobehavioral abnormalities found in FASD. In this review, the author discusses the mechanisms that are associated with FASD and provides a current status on the endocannabinoid system in the development of FASD.
人类孕期酒精暴露的一个独特特征是中枢神经系统（CNS）受损导致认知和行为功能受损，这会引发一系列被称为胎儿酒精谱系障碍（FASD）的损伤。孕期乙醇暴露后，啮齿动物的中枢神经系统可重现人类FASD表型。孕期酒精暴露对发育中的胎儿，尤其是发育中的中枢神经系统产生有害影响，预计有多种机制参与其中。这些机制可能同时或相继起作用，并且在特定脑区特定发育阶段的多种细胞类型中存在差异。研究已经确定了酒精作用于胎儿的众多潜在机制。这些机制包括氧化应激增加、线粒体损伤、对生长因子、神经胶质细胞、细胞黏附分子活性的干扰、中枢神经系统发育过程中的基因表达以及参与神经元通讯和回路形成的信号分子功能受损。这些酒精诱导的缺陷会导致神经元可塑性以及学习和记忆方面长期存在异常，并且可以解释FASD中发现的许多神经行为异常。在这篇综述中，作者讨论了与FASD相关的机制，并介绍了FASD发育过程中内源性大麻素系统的现状。
