Fetal Alcohol Spectrum Disorders (FASDs) describe a range of deficits, affecting physical, mental, cognitive, and behavioral function, arising from prenatal alcohol exposure. FASD causes widespread white matter abnormalities, with significant alterations of tracts in the cerebral cortex, cerebellum, and hippocampus. These brain regions present with white-matter volume reductions, particularly at the midline. Neural pathways herein are guided primarily by three guidance cue families: Semaphorin/Neuropilin, Netrin/DCC, and Slit/Robo. These guidance cue/receptor pairs attract and repulse axons and ensure that they reach the proper target to make functional connections. In several cases, these signals cooperate with each other and/or additional molecular partners. Effects of alcohol on guidance cue mechanisms and their associated effectors include inhibition of growth cone response to repellant cues as well as changes in gene expression. Relevant to the corpus callosum, specifically, developmental alcohol exposure alters GABAergic and glutamatergic cell populations and glial cells that serve as guidepost cells for callosal axons. In many cases, deficits seen in FASD mirror aberrancies in guidance cue/receptor signaling. We present evidence for the need for further study on how prenatal alcohol exposure affects the formation of neural connections which may underlie disrupted functional connectivity in FASD.

胎儿酒精谱系障碍 (FASD) 描述了一系列缺陷，影响身体、心理、认知和行为功能，由产前酒精暴露引起。FASD 导致广泛的白质异常，大脑皮层、小脑和海马的束显着改变。这些大脑区域出现白质体积减少，特别是在中线。本文中的神经通路主要由三个引导线索家族引导：Semaphorin/Neuropilin、Netrin/DCC 和 Slit/Robo。这些引导线索/受体对吸引和排斥轴突，并确保它们到达适当的目标以进行功能连接。在一些情况下，这些信号相互合作和/或与其他分子伙伴合作。酒精对引导提示机制及其相关效应器的影响包括抑制生长锥对驱避剂提示的反应以及基因表达的变化。与胼胝体相关，具体而言，发育性酒精暴露会改变 GABA 能和谷氨酸能细胞群以及充当胼胝体轴突路标细胞的神经胶质细胞。在许多情况下，在 FASD 中看到的缺陷反映了指导线索/受体信号传导的异常。我们提出了需要进一步研究产前酒精暴露如何影响神经连接形成的证据，这可能是 FASD 功能连接中断的基础。发育中的酒精暴露会改变作为胼胝体轴突路标细胞的 GABA 能和谷氨酸能细胞群和神经胶质细胞。在许多情况下，在 FASD 中看到的缺陷反映了指导线索/受体信号传导的异常。我们提出了需要进一步研究产前酒精暴露如何影响神经连接形成的证据，这可能是 FASD 功能连接中断的基础。发育中的酒精暴露会改变作为胼胝体轴突路标细胞的 GABA 能和谷氨酸能细胞群和神经胶质细胞。在许多情况下，在 FASD 中看到的缺陷反映了指导线索/受体信号传导的异常。我们提出了需要进一步研究产前酒精暴露如何影响神经连接形成的证据，这可能是 FASD 功能连接中断的基础。