Boschen K E, Klintsova A Y
University of Delaware, Newark, DE, United States.
University of Delaware, Newark, DE, United States.
Vitam Horm. 2017;104:197-242. doi: 10.1016/bs.vh.2016.10.008. Epub 2016 Nov 29.
Fetal alcohol spectrum disorders (FASDs) are a result of the teratogenic effects of alcohol on the developing fetus. Decades of research examining both individuals with FASDs and animal models of developmental alcohol exposure have revealed the devastating effects of alcohol on brain structure, function, behavior, and cognition. Neurotrophic factors have an important role in guiding normal brain development and cellular plasticity in the adult brain. This chapter reviews the current literature showing that alcohol exposure during the developmental period impacts neurotrophin production and proposes avenues through which alcohol exposure and neurotrophin action might interact. These areas of overlap include formation of long-term potentiation, oxidative stress processes, neuroinflammation, apoptosis and cell loss, hippocampal adult neurogenesis, dendritic morphology and spine density, vasculogenesis and angiogenesis, and behaviors related to spatial memory, anxiety, and depression. Finally, we discuss how neurotrophins have the potential to act in a compensatory manner as neuroprotective molecules that can combat the deleterious effects of in utero alcohol exposure.
胎儿酒精谱系障碍(FASDs)是酒精对发育中胎儿产生致畸作用的结果。数十年来,针对患有FASDs的个体以及发育性酒精暴露动物模型的研究揭示了酒精对大脑结构、功能、行为和认知的破坏性影响。神经营养因子在引导正常大脑发育以及成人大脑的细胞可塑性方面发挥着重要作用。本章回顾了当前的文献,这些文献表明发育期间的酒精暴露会影响神经营养素的产生,并提出了酒精暴露与神经营养素作用可能相互作用的途径。这些重叠领域包括长时程增强的形成、氧化应激过程、神经炎症、细胞凋亡和细胞丢失、海马体成年神经发生、树突形态和棘密度、血管生成和血管新生,以及与空间记忆、焦虑和抑郁相关的行为。最后,我们讨论了神经营养素如何有可能作为神经保护分子以补偿方式发挥作用,对抗子宫内酒精暴露的有害影响。